Maxillary Sinusitis of Odontogenic origin

Dr Elaine Cebuliak

Animal Wellness Veterinary Clinic, 700 Logan Rd, Greenslopes Shopping Mall Dental and Holistic Veterinary Referral Practice animalwellnessvets@gmail.com

Presentation Description:

Most veterinarians are (hopefully) aware that a facial swelling- or cheek abscess- is often caused by a draining periapical infection from an abscessing tooth, generally the upper premolar 4 or first molar. This is either from a primary or secondary periodontal problem or a fracture in the tooth. When the infection is unable to drain into the mouth or on the cheek, it can cause swelling, inflammation and discomfort into the nasal and paranasal or maxillary sinuses.

The author has found that in many cases of sneezing, reverse sneezing, nasal discharge , conjunctival inflammation, and ocular discharge: dental infections and inflammation have been involved, and are often missed during general clinical examinations . Careful attention to facial signs before examining the mouth may be helpful.

The author has seen cases where two or three primary access veterinarians with even extensive CT imaging and specialist internal medicine referrals have missed retained fragments of roots, which were surrounded by infected tissue and were obvious on dental radiographs.

A nidus of retained roots, alveolitis and dental disease is undervalued as a source of chronic infection and inflammation in this, which is also found in other author’s reviews. (2) This underlies a scenario found in the human medical profession. Search on Cochrane Library, PubMed and Science Direct data bases by key words resulted in 35 articles . It can be concluded that the incidence of odontogenic sinusitis is likely underreported in the available literature.

As the author is also a qualified Naturopath, she has sent some of her clients back to dentists to be investigated with dental radiographs and oral hygiene checks for sinusitis resolution with good effect. Ear Nose and Throat specialists also seem to ignore the oral cavity when it comes to dentition and apical infections, which is really not surprising when you consider that dentistry is a very specialised profession taking many years to understand the multiple areas within the profession.

The conclusion is that general practitioners need to be aware that dental disease can cause chronic upper airway infection and inflammation. If the doctor is presented with a chronic sneezing/nasal discharge sign it is important to use careful analysis of each and every tooth especially in the upper arcade, looking for crazes, fine fracture lines, periodontal pockets and stomatal inflammation.

Dental radiograph techniques need to be learned- and practiced, for well placed subgingival high resolution pictures that show “what lies beneath” . Digital radiographs are helpful as they can be magnified on computer screens which will find small retained root tips and loss of alveolar bone detail where infection is lingering. Plain intraoral radiographs can used and improved by placing them on an x-ray viewer and using a digital camera to take a picture of the hand developed dental radiograph. It can be enlarged for fine detail on a computer screen as a jpeg.

A literature review found several reports of odontogenic causative sinusitis in the human medical reviews.(1) A retrospective data analysis was performed on l 190 patients treated for unilateral

paranasal sinusitis . All patients were diagnosed based on clinical signs, symptoms, and imaging findings, including computed tomography (CT), orthopantomography (OP), and other modalities.

The most common cause of unilateral paranasal sinusitis was odontogenic infection, as seen in 138 cases (72.6%), followed by chronic inflammation in 43 cases (22.6%). Among patients diagnosed with odontogenic infection, one patient was also diagnosed with coexistent polyps and mycosis

CONCLUSIONS: Odontogenic infection involvement is implicated in sinusitis. Odontogenic maxillary sinusitis can be difficult to diagnose, and consideration of imaging performed under various conditions is recommended. In order to determine the most appropriate treatment for sinusitis, whether such treatment will be surgery, dental treatment, conservative therapy, or other treatments, collaboration between concerned doctors is essential.

1) Auris Nasus Larynx. 2015 Aug;42(4):288-93. doi: 10.1016/j.anl.2014.12.006. Epub 2015 Jan 28.Association between odontogenic infections and unilateral sinus opacification.Matsumoto Y1, Ikeda T1, Yokoi H2, Kohno N1.

2) Stomatologija. 2014;16(2):39-43.Odontogenic maxillary sinusitis: a review. Simuntis R1, Kubilius R, Vaitkus S.

Bones and Raw Food: What’s the Beef about Teeth? And other methods of home care.

Bones and Raw Food; What's the Beef about Teeth? and other methods of Home care.

Dr Elaine Cebuliak

Animal Wellness Veterinary Clinic, 700 Logan Rd, Greenslopes Shopping Mall Dental and Holistic Veterinary Referral Practice animalwellnessvets@gmail.com

Presentation Description:

Culturally feeding Raw Meaty bones (RMB) has been met as a dental challenge and an inappropriate method of providing dental hygiene for dogs and cats as seen by the veterinary dental establishment. However in many dog breeding groups and pet owning chat rooms, feeding RMB's is an acceptable practice. What are the drawbacks, risk factors, involved, and are there advantages to RMB's? How can we couch our wording to legally protect ourselves as informed care providers?

What should we feed our pets?

A balanced diet is one in which the micro (minerals, antioxidants, co-factors) and macro nutrients (carbohydrates, proteins, fats and water content) are provided at optimal levels. These levels contribute to periodontal health by providing antioxidants and trace factors for healthy collagen synthesis.

The consistency of the food product will vary depending on freshness, quality, and processing preparation. For dental hygiene to become optimal naturally abrasive, but not too abrasive, foods have been shown to clear plaque off the enamel coronal surface.

Recently the premium pet food companies have encorporated polyphosphates and fibre structure to act as plaque scrapers and digests.

Natural diets including raw meaty bones can be balanced and provide a beneficial diet for pets. There are many ingredients in natural raw/or semi fermented/cooked diets that are not available in heavily processed foods such as proteolytic enzymes Bromelain, papain, and probiotics. There are also some chemical untoward preservatives and substances lacking in natural raw foods--such as acrylamide, which is a known carcinogen that is formed with carbohydrates exposed to extreme heat and pressure, and are virtually present in all heat treated dried foods.(3)

Researchers in Europe and the United States have found acrylamide in certain foods that were heated to a temperature above 120 degrees Celsius (248 degrees Fahrenheit), but not in foods prepared below this temperature. (4)

Unfortunately there are incidences of calcium and phosphate imbalances when raw meaty bones are not provided as part of the diet, and where raw meat alone is substituted for commercial dry or tinned foods. Many a small breed is subject to the “chicken only” diet due to parental behaviour feeding problems.

When a carnivorous animal ingests the raw cartilage on the ends of the cancellous bone it also swallows and absorbs the matrix of the bone, that is collagen, proteins, and trace minerals necessary for its own bone growth. Daily homeostasis and joint motion involves a certain amount of metabolic catabolism and anabolism, (chondroblast/osteoblast vs osteoclast/chondroclast) structure is reflected by function due to piezoelectric stresses and strains on the skeletal system. Various studies have shown that daily ingestion of small amounts of glucosamine and chondroitin sulphate plus trace minerals Boron, Magnesium, Calcium, and Phosphates, impact favourably on the cartilage lost or

gained in the hyaline and endochondral plate of joint surfaces. The evidence supports supplementation of a diet with glucosamine and chondroitin in the human literature for knee osteoarthritis prevents joint space narrowing on radiographs (2)

Many dogs, especially of the smaller breeds not raised on chewing raw meaty bones will eat only meat as the owner offers. Vis:

An 8-month-old Shetland Sheepdog was evaluated because of the sudden onset of signs of neck pain, collapse, and inability to rise. A cursory diet history indicated that the dog had been fed a raw meat-based diet. CLINICAL FINDINGS: Initial evaluation of the dog revealed small physical stature, thin body condition, and signs of cranial cervical myelopathy. Radiographically, diffuse osteopenia of all skeletal regions was identified; polyostotic deformities associated with fracture remodeling were observed in weight-bearing bones, along with an apparent floating dental arcade. Hypocalcemia and hypophosphatemia were detected via serum biochemical analyses. The dog's diet was imbalanced in macronutrients and macrominerals. TREATMENT AND OUTCOME: The dog received supportive care and treatment of medical complications; neurologic abnormalities improved rapidly without intervention. Dietary changes were implemented during hospitalization, and a long-term feeding regimen was established Inadvertent malnutrition can be avoided through proper diet assessment and by matching nutrient profiles with patients' nutritional needs.

A Dentally abrasive diet which will clean teeth, and is balanced for micro and macrominerals is essential for good health. The right sort of raw meaty bone consistently and regularly introduced from a young age has been this authors experience in providing a great aid for periodontal health.

Why is it necessary to have "clean" teeth?

The biofilm that forms on the enamel surface of the tooth contains plaque; a glycocalyx of bacteria and a sticky glycoprotein that tenaciously grows upon itself, like a snowball. If this is not mechanically debrided by chewing adequately textured foods, or by toothbrushing, it becomes mineralized with the magnesium, calcium and phosphate ions present in saliva. This becomes calculus, commonly referred to as tartar. The bacteria and their toxins produce gingivitis, or inflammation of the gums, which is reversible with increased oral hygiene. If left unchecked it develops into Periodontitis which is:

The single most common affliction of pets greater than 3 years of age 90% pets >6yr.

Periodontitis (PD) is:

The cause of systemic illness - many people think that their pet is "just getting old" when in fact it is suffering chronic ill health. A transient bacteremia occurs when the (PD affected) pet bites or nibbles its fur, chews a bone, picks up a ball, or even swallows water. This will last for approximately 15 minutes and will be acted upon by the RES (reticuloendothelial system) to clear up the bacteria. Up to 15-20 thousand microbes per ml of blood locally are directly pushed into the blood stream This will seed microabscesses in the heart valve, liver, vertebral spine (spondylitis) kidney and other organs.

This will also cause a reduction in blood sugar (the bacteria metabolise this) and the animal will feel unwell, feverish intermittently, (often the cause of "FUO") and lethargic.

Progressive - If left unchecked the disease progresses. It is self perpetuating but episodic. The sulcular debris continue to release cytokines, complement is released by inflamed tissue, which attracts the cellular army of lymphocytes and neutrophils to phagocytose the debris and some of the inflamed tissue and the cascade continues to cause an increase in the depth of the periodontal pocket

Treating Periodontitis involves:

Scaling subgingival pockets and removing supra and subgingival calculus & Polishing teeth and gingival junction roots & interceptive orthodontics, exodontics where appropriate for crowding or furcation exposure, periodontal surgery, perioceuticals, Guided Tissue Regeneration, endodontics where pulpal involvement occurs and restoration of the coronal (crown) surface.

Oral pain prevents chewing & self cleaning; fractured teeth need repair (endodontics) or removal.

Do Bones Provide Enough?

Clients need to be informed that they cannot rely on bone chewing alone to clean all the surfaces of their pet's teeth. The ability of the pet to do this will depend on the anatomy of his/her mouth, the type of bone being offered, and the particular eating methods of the pet. Even “good chewers” develop plaque, especially on the buccal gingival surface of canine maxillary teeth.

A Dental Prophylaxis EXAMINATION is:

A Check for 'hot spots' in the mouth that may not self clean, particularly in an Orthodontically challenged mouth (e.g. 'undershot/overshot'), areas of persistent deciduous teeth, or a mouth that has crowded or rotated teeth. The problem areas in mouths vary from pet to pet. As a rule it is important to check the labial (outer, or lip) surface of the upper canines, the upper third and fourth Premolar, upper back molars (you need to really LIFT THE FLAP backwards for this!), and the lower molars.

How deep are your pockets?

An explorer tip to feel for secondary dentin versus exposed pulp, plus root surface calculus and furcation involvement and periodontal probing/measuring depth of pockets is essential. This can only be done with a general anaesthetic. A scale and polish procedure may be necessary in some animals once a year.

After a thorough dental prophylaxis (“prophy”)

TOOTHBRUSHING REMAINS THE GOLD STANDARD FOR HOME CARE!

What Advice do I give my client?

If home care is not in place all your efforts of dental prophylaxis are temporary. It is your duty, as the pet's Dental Technician, Hygienist, and/or Veterinarian, to teach the client an individualized and correct toothbrushing technique for these pets. I have found it necessary to provide lots of encouragement and support to the client in this area.

Often a general anaesthetic is necessary to be accurate in the assessment, as a periodontal probe will be required to measure periodontal pocket depths. This can be combined with the preliminary Scale, Polish and prophylaxis. After examining the pets' dentition, the client will need to be informed about supplementary brushing of particular areas. If these are too difficult for the client to keep clean (eg furcation involvement of upper molar or premolar teeth in otherwise sound immobile structures) consider extraction, or perioceutical placement of an antibiotic gel (eg doxirobe).

Other methods of home care include:

CET enzymatic chews, raw hides, Hill's TD diets, Eukanuba Dental defense foods, Kongchew toys, Tug toys, carrots, celery sticks, apples, Maxiguard oral gel, Dentabones. However the client should. supervise the use of these.

Tendons, pigs ears, and noses, and any dried meat that gets softer with a chew (not hooves as they are too hard and still break teeth) will work to reduce plaque. http://www.merrickpetcare.com/store/dog_treats_dental.php

Teaching the 'Brush off'

Many pets require a prophylactic dental scale and polish under a general anaesthetic before the client can begin to provide helpful tooth brushing. It is not possible to brush away deposits of calculus, and pets with painful mouths. Broken teeth, exposed pulp, or gingival sensitivities will not allow a toothbrush anywhere near them.

The system of praise and food treats in a healthy mouth for prophylactic brushing needs to be employed as positive reinforcement to make the learning experience work. It is pleasurable for the animal to have a clean mouth and most pets will look forward to their toothbrushing time, requiring very little persuasion.

Be regular. I tell the owner to practice the brushing technique several times a day until the pet is conditioned to the positive response. Once or twice daily brushing is often necessary, and it is important to set up a routine. Begin slowly with only one or two teeth, or even starting with the pet licking the toothpaste off the brush or finger stall. Reward. End positively with praise.

Make an associated location, eg. on top of the washing machine. Use an associated word with praise, eg "tooth-time" and lots of pats, treats "good tooth-time" in the higher pitched happier voice. Praise lavishly. Use tasty food rewards liberally, liver Jerky snax, pate', freshly cooked chook pieces, cheese. Use a finger stall brush with pleasant tasting tooth paste for animals - human ones 'burn' the mouth, are unpalatable for pets, and are meant to be rinsed out.

Graduate to a small head toothbrush to reach the distal teeth surfaces after 2-3 weeks. It may not be necessary to open the mouth, often only the lateral (buccal) areas require brushing. Rotary/ motorised (electric) toothbrushes save time and do an excellent job once the pet is trained to accept this.

Plaque comes back!

Three Free:

Client's efforts need to be evaluated and praised, as in any training of a new technique or motivation will wane. Looking after their pet is a taught and learned behaviour, many nuances and slight changes in body positioning, tonality of voice and calming techniques help in obedience training. Toothbrushing is no different to teaching a dog to sit.

I recommend the general practice engages a dental nurse to have three free oral hygiene rechecks, usually spaced 1 week after the dental prophylaxis, then 1-month, then 2- months. These can be performed by a well trained veterinary nurse, or ancillary staff.

Do you visit your Dentist only every 14 years? This would be the same as checking the teeth every 2 years. Even 6 monthly checkups may be too sporadic in difficult cases of periodontitis, where 3 monthly checkups would be better.

Regarding Bones:

Many Veterinarians are concerned about the possibility of having raw meaty bones contribute to fractured teeth, notable the PM4 uppers or Carnassial Maxillary teeth. If the bones are chosen carefully for having a large percentage of cartilage and sinew and are not cut or split (ie. chop bones) this risk is minimal and does not seem to outweigh the benefit for superior periodontal health provided by a “good chew”.

It is interesting to note that there is a large cultural bias regarding the subject of bone chewing for pets. In the United States, a country more litigious than Australia, many veterinarians actively discourage feeding bones.

Clients rely on the advice of their Veterinarian and Technician and it is possible that Murphy's law may pervade. Therefore, when giving any advice some Veterinary Defence agencies recommend disclaimers and waivers are signed by the client, and these are stored for future reference. You may document your advice given during the consultation in your software based word programme to the effect of “Mrs Jones was advised that she must supervise raw meaty bone chewing, and once the bone becomes small enough to choke or the hard shaft of a bone is left it must be removed as it may cause enamel fractures”

Are bones harmful? Bones have been implicated in causing:

Pancreatitis - especially common in overweight animals. The marrow of the bone, and some parts on the outside represent 99% fat. Many dogs have sedentary lifestyles and cannot tolerate this heavy fat intake, especially the small breed dogs where such a high caloric intake in one sitting may send it’s inflamed pancreas over the edge. It is important to trim off the fat and not feed bones that are sliced open by the butcher to allow access to the marrow. This shape has also been linked to mechanically fracturing the upper carnassials, as has chop bones wedged in the lower molar. Pancreatitis and liver upsets can occur from overzealous ingestion of the fat.

Bones can get wedged in the top of the palate. Chicken necks and small bones can choke or cause oesophageal blockages. This, however

is true of any ingested shape, such as greenies. (6) Bones can break the carnassial (upper premolar 4) of the dog's top jaw. Chop bones can get wedged cause pain, periodontitis, and fracture the lower teeth. Bones must NEVER be cooked, as they can lodge in the intestine, stay undigested and cause

constipation, perforation, peritonitis and death. Bones, especially raw chicken, can be a source of salmonellosis. This especially significant in

PAT (pets as therapy) dogs that visit hospitals, nursing homes etc where fragile patients are exposed and pat the carrier. It is important to note that this is not confined to RMB alone, as Pedigree (Mars) pet food was recalled for this reason in the USA in 2008. (5)

The 'Useful Chew'

FEED BONES THAT HAVE CARTILAGE AND SINEWY MEAT AND SOFT, CANCELLOUS (CHEWY) BONE. THROW THE BONE AWAY AFTER a suitable time period - this varies for each individual dog, when the chewing has taken off the meat and cartilage. If your dog doesn't have appropriate chewing behaviour (eg. some Bull terriers and Labradors) you must be extra vigilant. Most of our pets are overfed; remove all the fat first. Helpful tips for removing the bone include taking the dog for a walk or otherwise distracting it to come inside the house or play ball/toy.

Therefore we recommend careful assessment of each individual and each animal for their ability to handle bones. Forewarn clients of some inherent dangers.

1) Do not give cooked bones

2) Cut off fat

3) Supervise bone chewing, removing bone after the 'useful chew' stage

4) Choose the appropriate size for the dog/cat

5) Choose bones with cartilage and sinew

6) Do not give chop or split shaft bones

7) Perform a baseline anterior abdominal palpation and serum lipase and amylase for suspect pancreatitis patients. If the patient has a history of pancreatitis-- recently (in the last 2 months) then aim for no bones for a month, and increase the antioxidants, add cardamon, citrus peel, turmeric, ginger (all in small amounts) and vegetable matter to the chicken and rice diet. Stop all fat. Limit the raw meaty bone access to chewing to 2-3 times a week for only 10 minutes, and heavily supervised. Remove all possibility of large chunks being swallowed. Make sure the bones have lots of cartilage and sinew and are not cut in half longitudinally where the bone marrow could be accessed, as this is 90+% fat.

HAPPY BRUSHING!

Other Pet food Pitfalls:

It must be noted that there have been problems encountered with both commercial or “professional” diets as well as Raw/homemade diets :

Commercial: Contamination with toxic chemicals, irradiation producing free radicals

1. Orijen pet foods imported into Australia in 2008 were linked to neurological deficits especially in cats that were fed their irradiated imported foods. Champion Petfoods announced the voluntary recall of its ORIJEN brand cat food sold in Australia. Also, as it appeared that at least 2 cats have suffered from ingesting Orijen Dog

This food was irradiated when it enters Australia – irradiated food may be higher in free radicals which are damaging to tissue, and lower in anti-oxidants and Vitamins

2) Gluten contamination with Melamine:

Menu Foods Inc. (and others), a Canadian manufacturer of wet pet food, recently recalled more than 60 million containers of cuts and gravy-style food from two U.S. facilities because of concerns about the effect of the products on the renal health of pets.

The FDA, which regulates pet food and many ingredients in pet food, stated that the recall resulted from consumer complaints and the deaths of animals in routine palatability studies. A suspect agent at press time in late March was melamine, which had apparently contaminated the wheat gluten that went into food that was recalled.

This contamination affected many of Nestle products around the world, and American citizens may be unaware of the impact this had on baby formulae in third world countries. Even white chocolate “rabbits” in New Zealand were affected. Furthermore most Pet food manufacturers sourced their common ingredient of Wheat Gluten (which binds kibble) from the same Chinese manufacturer, indeed we have no idea as consumers how far reaching this melamine has travelled. One may even say that these toxic ingredients are the equivalent of the 9/11 in the pet food world.

3) Preservatives such as BHA, BHT, Ethoxyquin, and “Food colouring” made out of tartrazine yellow dyes, allergenic Carmine red dyes (Crimson Lake, Cochineal, Natural Red 4, C.I. 75470, or E120, is a pigment of a bright red color obtained from the carminic acid produced by some scale insects, such as the cochineal), coal tar substances and other potentially toxic ingredients are present in most commercial food, which need to have long shelf lives to make a profit. Studies have found that BHA can produce allergic reactions and, in larger doses, affect liver and kidney functions. The oxidative characteristics and/or metabolites of BHA and BHT may contribute to carcinogenicity or tumorigenicity. Dr Tomoyuki Shirai, chairman of the Department of Pathology at Nagoya City University Medical School in Japan, who revealed the results of a recent study done on rodents to determine the toxicology of BHA, BHT and ethoxyquin. Ethoxyquin, BHA and BHT are carcinogenic in

rodents, ethoxyquin significantly increased the incidence of stomach tumours and colon tumours, enhanced bladder carcinogenesis and pronounced kidney carcinogenesis.

The study revealed that BHA caused carcinomas in the stomach of the rodents and enhanced cancer of the stomach and urinary bladder. BHT was found to promote cancer of the urinary bladder and a possible thyroid cancer. (12)

4. Gluten alone can cause IBS/IBD and contribute to atopy via the “leaky gut syndrome” also known as translocation, where larger protein molecules can transfer through the inflammed intestinal patches into the blood stream. Most commercial foods use Gluten as the binder for their kibble (15) Gliaden and gluten proteins are known molecular mimicry compounds and set up autoimmune reactions such as hashimoto’s thyroiditis. Furthermore it is not necessary for the pet food industry to label the gluten content on their foods, and even ‘grain free” kibble may use gluten as a binder, so owners attempting to feed a gluten free diet may not be able to realistically avoid this substance.

5. Acrylamide -a known carcinogen- is released with heating carbohydrates to high temperatures. Acrylamide, and various pyrroles have been found in most foods heated at high temperatures and there is evidence of carcinogenicity in experimental animals (14)

6. Some of the cheaper inferior kibble/ age inappropriate food can be insufficient in trace minerals and vitamins. Rickets was diagnosed in six 14-week-old racing greyhound littermates presented with musculoskeletal disease.(10) Physical findings included listlessness, profound muscle weakness, lameness, lateral bowing of the antebrachii and focal hard swellings proximal to the tarsi and carpi. Radiological findings included generalised osteopenia, axial and radial thickening of growth plates, and "cupping' of the adjacent metaphyses; the distal ulnar growth plates were most severely and consistently affected. The diagnosis was confirmed by demonstrating subnormal concentrations of 25-hydroxycholecalciferol in serum samples collected at admission. The pups' diet consisted of an inexpensive generic kibble formulated for adult dogs, porridge, milk, pasta, minced beef, vegetables and a small quantity of calcium carbonate powder.

7. Soya phytates – often called TVP or Textured Vegetable Protein are a major ingredient in many pet foods and can combine in the gut with minerals such as (zinc) zn and make these unavailable for absorption over time, contributing to ill health and zn deficiency.

8. GMO- Genetically Modified Organisms in the food chain are engineered food crops particularly in varieties of sorghum, maize /corn and wheat. They were specifically designed to produce insect repellent properties or to be able to resist monsanto’s weedkillers such as the glycosphate round up. These disturb the respiration cycle of the insects known as the Shikimate pathway, and because mammals do not have this pathway (instead the glycolytic pathway and TCA or Krebs cycle is used in mammals) so it was thought mammals would not have a problem with ingesting these food sources. However mammalian bodies are actually 90% bacteria and only 10% mammalian- that is their gut and skin is colonised by bacteria that are useful and symbiotes. These GMO seeds have become known as “Round up ready” and as such disturb the gut flora of mammals, causing a gut dysbiosis and leaky gut. Many of our autoimmune patients and patients with IBS/IBD are actually showing signs of GMO toxicity.

Natural and Raw Diets:

BARF (Bones and Raw Food) diets have been popular in Australia forever, as dogs raised on outback properties were fed fresh roo kill and mutton leftovers from the kill. They have certainly gained credence in suburbian backyards since Dr Ian Billinghurst wrote his 2 books: “Give Your Dog a Bone” and “Grow Your Pups With Bones”. The Raw Meaty Bone debate continues to this day around the globe, with the likes of Dr Tom Lonsdale presenting his Pet food causes an “Aids like illness” theory of periodontal disease; leading to some major political battles within the Australian Veterinary Profession and the Pet food industry which are legendary. Although Dr Tom’s published (JSAP) data relating to the feeding of tinned/canned soft foods did show chronic lymphocytic and a leukopenic (Dr Tom sensationally referred to this as “AIDS-like”) responses, these foods were not dentally abrasive, nor did they contain elements to reduce plaque. It may be that feeding pap was a textural problem contributing to dental disease, plaque accumulation and periodontitis. Perhaps this lead to the invention of the Dental Kibble?

“An article published in the December 1995 issue of the British Journal of Small Animal Practice confirms that processed pet foods produce periodontal disease which often leads to an AIDS-like condition in affected animals. ( JSAP 1995 36, 542-546 ) Dr Tom Lonsdale of Riverstone NSW the author of the paper admits that he, along with almost everyone else, used to recommend processed pet foods. "Previously we thought animals were suffering the effects of old age when in fact they were wasting away with periodontal disease and diet-induced AIDS." "Now we treat the periodontal disease and provide the pets with a natural diet. The removal of the poisons allows the immune system to recover and owners frequently report that their old pet is like a puppy/kitten again." "I believe that this information should have been available to Australian vets and their patients in 1993. The Australian Veterinary Journal refused to publish the research findings." (17)

Ian Billinghurst’s book was launched at a 3 day Bichon Frise conference in western Sydney on the 17th November 1993 and was advertised in all the canine breeder magazines throughout Australia. It deals exclusively with feeding dogs their natural or evolutionary diet

The theory of the “evolutionary diet” is that man and dog first formed a friendship back in the cave man era (250,000 years ago), forged by a symbiotic relationship of combined hunting skills, early warning of danger and protection, companionship, and the cleaning up of all man’s food scraps and waste. “Man’s best friend” has continued to provide this service throughout the history of mankind; his role as hunter, pest controller, scavenger and waste disposal provided the dog (and cat) with its natural diet of raw meats and scraps. It was not until just over 30 years ago in Australia that the first commercial cooked dog and cat foods were released onto the market….and with that some practitioners claim, began the slow and insidious decline in health of modern day dogs and cats.

The average veterinarian today spends more than half his or her working day treating the epidemic of skin diseases, allergies, arthritis, teeth and gum problems, ear infections, anal gland impactions, urinary tract diseases and a huge range of degenerative diseases and cancers previously only thought to occur in man.

It is this background of information that lead Australian veterinarian Dr Bruce Syme to begin searching for a solution to this health crisis that did not depend on the continuous use of drugs like cortisone and antibiotics ( and the need for more drugs to counter the side effects of the original treatments). “ It was simply out of frustration, as a vet, that lead me to look for a better answer to these problems. I was embarrassed every time my clients came back for more consultations and more drugs for the same old problems..itchy skin, ear infections, arthritis therapy etc..” And the answer to these problems…nutrition.

The solution is as simple as the statement “dogs and cats can’t cook !! ”. Dr Syme, along with a growing body of vets, breeders, and every day dog and cat owners, and a wealth of scientific evidence, believes that it is the practice of feeding cooked and processed pet foods, that has resulted in the dramatic decline in health of modern dogs and cats.

Cooking food does a lot more than just destroy vitamins, it changes the molecular structure of food, and destroys essential fatty acids, denatures proteins and enzymes, damages minerals and micronutrients, and severely decreases the nutritional content of any food source. It can actually produce carcinogenic elements if the cooking temperature is high enough . In reverse, the feeding of a natural, raw food diet, consisting of raw meats, grains, vegetables, fruits and other supplements, can prevent, and actually “cure” many of the common health complaints mentioned above.

Some of the inherent problems in home-prepared/raw foods are:

1. Pathogenic bacteria and their toxins may be present, such as Salmonella, E. coli, Clostridium sp. Pets as therapy require “clean” rectal swabs.

2. Imbalances in mineral content- especially if NOT fed raw meaty bones, hyperphosphatemia and rickets have been noted

3. Lack of fibre if fruit and vegetables are not added. This causes intestinal dysbiosis (low probiotics) if poor in prebiotics.

4. Imbalances in protein/carbohydrate/ energy and growth for life stages

5. Table scraps may be an unfortunate mix of too much fat and cause pancreatitis.

6. Always avoid cooked bones! They splinter and are undigestable leading to lacerations and perforations of the intestinal mucosa, also too many raw bones can still lead to constipation.

Legal Implications:

How can we couch our wording to legally protect ourselves as informing care providers?

Jurisprudence requires that we must give our clients the best advice for their pet care that will cause no harm. In many instances there are positives and negatives associated with our feeding choices. It may be appropriate for vets to have handouts elucidating the various pitfalls of both raw and commercial foods to allow clients to make up their own decisions.

The Class action that was filed against the melamine tainted pet foods is still being resolved. This is a proposed settlement of the class action lawsuits known as In Re: Pet Food Products Liability Litigation, MDL Docket No. 1850, Civil Action No. 07-2867 (NLH) (All Cases) that are pending in the U.S. District Court for the District of New Jersey and similar lawsuits pending in Canada.

This proposed Settlement Agreement is with various companies and persons or entities that handled, distributed, purchased for resale and/or redistribution, supplied, manufactured and/or sold or offered for sale pet food and/or pet treats that may have contained contaminated wheat gluten or rice protein concentrate and were recalled beginning in March 2007, as well as certain companies, persons or entities that supplied that wheat gluten or rice protein concentrate ("Recalled Pet Food Products"). The settlement includes the United States and Canada.

On November 18, 2008, after a full-day Final Approval Hearing, Judge Hillman issued an Order and 65-page Opinion approving the Settlement and denying all objections to the Settlement. Appeals have since been filed by two separate objectors contesting final approval of the Settlement, and these appeals will postpone the payment of claims. No payments may be made on eligible claims until all appeals are resolved. THE APPEALS HAVE BEEN FULLY BRIEFED, A HEARING WAS HELD ON FEBRUARY 22, 2010 AND WE NOW AWAIT THE DECISION OF THE APPELLATE COURT. It is uncertain how long these appeals will take to resolve, and the timing of resolving the appeals is not within the control of the parties or their counsel. It is not uncommon for appeals to take several months or even years to resolve. (13)

If our dental diets (either raw, cooked or commercial) are not balanced or have been shown to cause intestinal blockages or contain toxic/parasitic ingredients perhaps, in a litigious world, we need to be cognisant of this and have a proforma disclaimer so the client is aware of potential pitfalls.

No one diet will fit all pets, and any changes in diet, especially to BARF will require gradual transitions and careful monitoring while the gut flora become balanced.

References:

1. J Am Vet Med Assoc. 2009 Apr 15;234(8):1041-8.Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef.Taylor MB, Geiger DA, Saker KE, Larson MM.Banfield, The Pet Hospital, Christiansburg, VA 24060,

2. http://findarticles.com/p/articles/mi_m0689/is_3_52/ai_99254316/Do glucosamine or chondroitin cause regeneration of cartilage in osteoarthritis? Journal of Family Practice, March, 2003 by David Priebe, Todd McDiarmid, Leslie Mackler

3. http://www.rsc.org/chemistryworld/News/2007/December/05120703.asp 4. http://www.cancer.gov/cancertopics/factsheet/risk/acrylamide-in-food 5. http://petcare.suite101.com/article.cfm/salmonella_in_cats_and_dogs 6. http://www.pantagraph.com/news/article_0b6a80d7-c358-55bd-89f3-de4cad24b486.html

greenies and other choking treats 7. http://www.pharmainfo.net/guptashubhranshu/toxic-food-additives-part-v-bha-bht 8. http://en.wikipedia.org/wiki/Wheat_allergy 9. Acta Dermatovenerol Croat. 2010;18(1):38-55. 10. J Small Anim Pract. 1997 Mar;38(3):109-14.

Rickets in a litter of racing greyhounds.Malik R, Laing C, Davis PE, Allan GS, Wigney DI.Department of Veterinary Clinical Sciences, University of Sydney, New South Wales, Australia.

11.Role and significance of atopy patch test.Jurakić Toncić R, Lipozencić J.University Department of Dermatology and Venereology, Zagreb University Hospital Center and School of Medicine, Salata 4, HR-10000 Zagreb, Croatia. 12.www.dogslife.com.au/dogs_life_articles?cid=9439&pid=150293 13.http://www.petfoodsettlement.com/ 14.Int J Cancer. 2009 Mar 1;124(5):1196-9.Long-term dietary acrylamide intake and risk of endometrial cancer in a prospective cohort of Swedish women.Larsson SC, Håkansson N, Akesson A, Wolk A.Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. susanna.larsson@ki.se 15.Neuro Endocrinol Lett. 2008 Dec;29(6):902-10.Normalization of leaky gut in chronic fatigue syndrome (CFS) is accompanied by a clinical improvement: effects of age, duration of illness and the translocation of LPS from gram-negative bacteria. Maes M, Leunis JC 16.Curr Opin Immunol. 2009 Feb;21(1):111-7. Epub 2009 Apr 1.Antigen presentation in celiac disease.Qiao SW, Sollid LM, Blumberg RS.Centre for Immune Regulation, Institute of Immunology, Rikshospitalet University Hospital and University of Oslo, Norway. s.w.qiao@medisin.uio.no 17. Media Release 17 March 1996. Permission to reprint from Dr.Tom Lonsdale NSW 18.Hanaa A. S. Oraby, Mahrousa M. H. Kandil, Amal A. M. Hassan, Hayam A. Al-Sharawi (2014) Addressing the issue of horizontal gene transfer from a diet containing genetically modified components into rat tissues. Afr. J. Biotechnol. Vol. 13 No. 48 http://www.academicjournals.org/journal/AJB/article-full-text/BE5331948800 19. CHAINARK, P., SATOH, S., HINO, T., KIRON, V., HIRONO, I. and AOKI, T. (2006), Availability of genetically modified soybean meal in rainbow trout Oncorhynchus mykiss diets. Fisheries Science, 72: 1072–1078. http://onlinelibrary.wiley.com/doi/10.1111/j.1444-2906.2006.01258.x/abstract 20. Chainark P, Satoh S, Hirono I, Aoki T, Endo M. (2008) Availability of genetically modified feed ingredient: investigations of ingested foreign DNA in rainbowtrout Oncorhynchus mykiss. Fisheries Science.74:380390 http://onlinelibrary.wiley.com/doi/10.1111/j.1444-2906.2008.01535.x/abstract 21.Hanusova L., Rehout V., Citek J. (2011) Transgene Fragments in the Blood and Tissue of Chicken Fed with Genetically Modified Soy and Maize. Animal Nutrition and Feed Technology, 2011, Volume : 11, Issue : 2 page 249-256 http://www.indianjournals.com/ijor.aspx?target=ijor%3Aanft&volume=11&issue=2&article=012

22. Ran T, Mei L, Lei W, Aihua L, Ru H, Jie S. (2009) Detection of transgenic DNA in tilapias (Oreochromisniloticus,GIFT strain)fed genetically modified soybeans (Roundup Ready). Aquaculture Research. 40:13501357 http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2109.2009.02187.x/abstract 23. Tao Ran, Liu Mei, Wang Lei, Jiang Keyong, & Wang Baojie. (2009). Tissue Studies of Tilapias fed with Transgenic Soybean Feedstuff. Inspection and Quarantine Science , 19 (2), 22-25. http://www.cqvip.com/qk/98475a/200902/30285206.html 24. Řehout V., Hanusová L., Čítek J., Kadlec J.., Hosnedlová B (2008) Detection of DNA fragments from Roundup Ready soya in blood of broilers Journal of Agrobiology, 25: 145-148 http://binoz.biol.uni.torun.pl/binoz/binoz/pareek-pdf/pareek2008-3.pdf#page=147 25. Tudisco R., Mastellone V., Cutrignelli M.I, Lombardi P, Bovera F., Mirabella N., Piccolo G., Calabro S., Avallone L., Infascelli F.(2010)Fate of transgenic DNA and evaluation of metabolic effects in goats fed genetically modified soybean and in their offsprings. Animal.The Animal Consortium:1-10;4:1662-1671 http://www.ncbi.nlm.nih.gov/pubmed/22445119 26. R. Tudisco, M. I. Cutrignelli, S. Calabrò, A. Guglielmelli, F. Infascelli (2010) Investigation on genetically modified soybean (RoundUp Ready) in goat nutrition: DNA detection in suckling kids. Italian Journal of Animal Science, Vol 6, No 1s 380-382 http://aspajournal.it/index.php/ijas/article/viewArticle/ijas.2007.1s.380 27. R. Tudisco R., Calabrò S. Cutrignelli M.I., Moniello G., Grossi M., Mastellone V., Lombardi P., Pero M., Infascelli F. (2015) Genetically modified soybean in a goat diet: Influence on kid performance, Small Ruminant Res. http://www.sciencedirect.com/science/article/pii/S0921448815000528 28. Khulod Ibraheem Hassan, Ali Abdulla Ali (2012) Detection of Genetically modified DNA in Milk Using Species Specific PCR Journal of American Science 8(9) http://www.jofamericanscience.org/journals/am-sci/am0809/036_10402am0809_248_252.pdf 29. Vincenzo Mastellone, Raffaella Tudisco, Giovanni Monastra, Maria Elena Pero, Serena Calabrò, Pietro Lombardi, Micaela Grossi, Monica Isabella Cutrignelli, Luigi Avallone, Federico Infascelli (2013) Gamma-Glutamyl Transferase Activity in Kids Born from Goats Fed Genetically Modified Soybean Food and Nutrition Sciences, 4, 50-54 http://dx.doi.org/10.4236/fns.2013.46A006 30. Chowdhury EH, Kuribara H, Hino A, Sultana P, Mikami O, Shimada N, Guruge KS, Saito M, Nakajima Y. (2003) Detection of corn intrinsic and recombinant DNA fragments and Cry1Ab protein in the gastrointestinal contents of pigs fed genetically modified corn Bt11. J Anim Sci. 2003 Oct;81(10):2546-51. http://www.ncbi.nlm.nih.gov/pubmed/14552382 31. Netherwood T., Martín-Orúe S.M., O’Donnell A.G., Gockling S., Graham J., Mathers J.C., Gilbert H.J. (2004) Assessing the survival of transgenic plant DNA in the human gastro- intestinal tract. Nature Biotechnology 22, 204-209 http://www.ncbi.nlm.nih.gov/pubmed/14730317  

Oronasal fistula saga- a case report.

Dr Jessamy Alexander, BVSc (Hons) MRCVS (Dentistry and Oral surgery).

Lecturer at the University of Melbourne Veterinary Hospital, Faculty of Veterinary Science, 250 Princes Hwy, Werribee, Victoria 3030, Australia

This case presentation is a follow up to the paper published in the Australian Veterinary Practitioner, Volume 44 (4) September 2014, page 673, entitled:

“Malocclusion causing a traumatic oro-nasal fistula and secondary rhinitis in a dog”.

Fitzgerald WE, Alexander JR

Summary:

The reason for the initial presentation of a male, long haired Weimaramer, at 7 months of age, was primarily a right-sided nasal discharge that was secondary to a mandibular distocclusion that placed the mandibular canine teeth distally and palatal to the maxillary canines. The crown of the right mandibular canine tooth (#404)i had penetrated the palatine mucosa and hard palate creating an oronasal fistula (ONF). Treatment involved addressing the malocclusion, by crown amputating the mandibular canine teeth, and closing the fistula with a sliding palatal flap. This was repeated at 11months, and again at 1 year 3 months of age, following a breakdown of the repair. This repair was considered successful and the flap fully healed.

The dog presented at 2 years and 1 month for castration, with a request to examine the hard palate. At this time it was identified that an ONF had reoccurred. It should be noted that at no visit was it possible to open the dog’s mouth for a conscious examination, this required either sedation or general anaesthesia. Surgery was performed 4 weeks later, using harvested auricular cartilage to create further support to the palate repair in the absence of the underlying bony hard palate. At recheck 1 week later, the repair had broken down.

1 week after this a (fourth) repair was performed using a sliding palatal flap, and at thus time it was concluding that due to a mild wry bite, #403 and possibly #403 had contributed to breakdown of the flap, These teeth were extracted. At recheck for this repair 1 week later, then was some break down in the rostral section, with organic debris (grass seeds) caught in this area. Sutures were still intact, and after removing foreign bodies, reparation was made.

Case:

A seven-month old male dog with right-sided nasal discharge was presented, the owners were aware that it had a malocclusion when purchased as a young puppy but unaware that it was the primary cause of the rhinitis. Because of the severity of the malocclusion (mandibular distocclusion, confirmed along with secondarily linguoversed mandibular canine teeth) and the consequent palatine trauma, it was considered unreasonable to delay treatment but to relieve the traumatic occlusion immediately. The dog was admitted for a thorough examination and to determine the most appropriate treatment.

In this case, a crown amputation procedure was proceeded with and a surgical palatal flap was made to close the fistula. Crown amputation (with vital pulpotomy) was the treatment of choice in this case,

as the mandibular teeth were positioned so far distally that it was not considered feasible to orthodontically move them into an appropriate ‘canine interlock’ position (thus relieving the traumatic occlusionii,iii,iv). Crown amputation was considered preferable to extraction, allowing the tooth to continue to give strength to the mandible, and if performed aseptically by an experienced operator, success rates of this elective procedure are reported to approach 100%v. The mandibular canine teeth (#304 and 404) were not yet mature, as was indicated by their open apicesvi, and had erupted asymmetrically: It was thought that the eruption of #304 had been truncated because of its contact with the palate whereas #404 had continued to erupt and was responsible for the complete penetration of the palate.

Deep impressions into the palatine mucosa made by contact from the mandibular incisor teeth were documented and photographed at this and subsequent times.

Dental radiographs demonstrated significant palatal bone loss in the vicinity of the right palatine fissure; the result of this was that any palate mucosa reconstruction would be unsupported (by bone).

A full thickness, palatal sliding flap was constructed to close the right-sided oro-nasal fistula: a number-11 scalpel blade was used to make a ‘U’ shaped incision: midline, rostral and palatal to the right maxillary canine tooth, leaving the flap attached distally. This tissue was elevated using a sharp periosteal elevator trying to avoid the palatine vessels that approach distally in and enter through the palatine fissures. To relieve tension, elevation of the palatine mucosa was continued until the flap could be comfortably opposed to cover the deficit. The flap was rotated buccally to close the fistula, leaving the midline longitudinal incision in the palate close to the midline; this deficit was not sutured but left to granulate. vii , viii. The palatine mucosal tissues were very inflamed and diffuse vascular bleeding was significant however this subsided with several minutes of applied digital pressure. Closure was with sutures in a simple interrupted pattern (Monosyn suture, 4/0 taper-trochar point DRT18, Code: C0022344. Braun, Aesculap AG & Co.).

At revisit approximately 4 months later (11 months of age) the right nasal discharge had reoccurred requiring re-closure of the fistula. This was again done with a sliding palatal flap. At this stage the crown amputations/ vital pulpotomies were checked by X-ray- there was narrowing of the pulp cavity, and dentinal bridges were present. Nasal scope was performed to check for other foreign material (none being present).

By 1 year and 3 months of age, the ONF had reoccurred. It appeared as though there were two fistulas alongside each other, causing the deficit. Dental X-ray showed continued and significant loss of supporting palatine bone. A sliding palatal flap was performed similarly to the previous procedures. The mandibular canines #304 and #404 were suspected to have erupted further, and now appeared proud of the adjacent incisors. Further shortening the mandibular canine teeth was performed- approx. 2-3mm was removed from the crowns of each tooth, then restoration repeated (note the pulps were not exposed when this small amount was removed, as the dentinal bridges formed a solid “floor”).

10 months later (2 years and 1 month of age), when being checked at the time of castration, it was noted that an ONF was present again. However, this ONF was more rostral to the original fistula created by the canine tooth. Further bone loss of the hard palate, was noted on dental X-ray. The deficit appeared to be, more medial and rostral than the original ONF.

At this stage, a different approach was decided upon, since “trampoline effect” was considered one of the more likely reasons for the ONF to have reoccurred. The trampoline effect refers to pressure over soft tissue, when it is unsupported by normal structures- in this case, the palatal bone. On questioning of the owner, it was found that, contrary to dietary and behavioural advice, the dog was being fed chews including raw chicken carcasses. This was largely responsible for the foreign material removed from the dog’s right nasal passages at each examination and likely a significant aggravating

factor to the health of the repairs. It was thought that more support and strength was required in the area, so the ONF was repaired using auricular cartilage sutured into the deficit (between residual bone and the palatal mucosa) ix, x. Again, repair utilized 4-0 monosyn, combination of simple and horizontal mattress sutures. However, at recheck 1 week later, the site had again broken down.

Two weeks after the auricular cartilage repair (the dog was now 2 years 2 months of age), the dog was again placed under general anaesthetic for another repair. The plan was at this stage was to extract #103 and create a large mucogingival flap to close the palatine deficit. However, surprisingly, due to significant healthy granulation tissue development beneath the palate in the area of the bone deficiency, the ONF had reduced in size. Again, this made a sliding palatal flap the treatment opted for. Significantly, it was considered at this time that #402 and #403 might have been interfering with the wound site, due to the mild wry bite. The crown of tooth #403 corresponded exactly with the new fistula whereas the original fistula site (corresponding with tooth #404) had healed. Incisors #402 and 403 were extracted. In an attempt to reduce interference with the healing site even further, a figure 8 wire was placed around the maxillary canine and was bonded to the canines with a composite, and the wire lifted off the palate so it did not contact the palate at all. The areas where the mandibular canines would contact it were filled with Protemp Garant, in a similar fashion to the construction of a maxillary plate with bite planes. The aim being to remove any mandibular contact with the dog’s palate. Despite the apparent strength of the apparatus, the dog managed to damage the plate during its recovery, and thus the apparatus was removed.

At the 1 week recheck, this flap was noted to be still in place, but grass seeds had penetrated the rostral section which had not yet healed. The sutures were all still present. Further sutures were placed. The extraction sites of the incisors had healed well. A recheck was planned for 2 weeks later.

At this recheck the site had healed except for a very small deficit (1mm diameter) surrounded by granulation tissue. No further follow up was planned.

Discussion:

Material found in the ONF:

1st exam (7 months old): Fluff, fabric, grass and bone.

2nd exam (11 months old) : Fluff, fabric, grass.

3rd exam (1 year 3 months old): Hair, fabric, grass.

4th exam (2 years 1 month old) : Small pieces of bone (suspect chicken bones), grass, hair, and necrotic meat like material.

5th exam (2 years 2 months old) : Necrotic meat like material, grass, fluff (possibly from bedding).

6th exam: As above

This is of interest as it gives an idea that the owner had stopped, then restarted feeding bones post repair. It also indicates the nature of the dog to chew on anything it can find, making it difficult to completely prevent all interference with the healing site.

Reasons for failure:

1st treatment (7 months of age)

Procedures performed: GA. Sliding palatal flap and crown reduction of #304 and #404.

4 months later, this surgery was noted to have partially failed- possibly due to:

Complications arising from the inflammation of these tissues at the time Too much tension/ flap not large enough. From patient interference. (chew items and play with another dog).

2nd treatment (11 months of age)

Procedure performed: GA. Sliding palatal flap. Repeat X-rays of #304 and #404.

4 months later, the ONF had reoccurred - possibly due to:

The continued eruption of the mandibular canines. The apices were noted to be open at the time of crown amputation.

Sliding flap with too much tension. From continued patient interference (chew items and play with another dog).

3rd treatment (1 year 3 months of age)

Procedures performed: GA. Full thickness sliding palatal flap, larger, more aggressive than the first two. #304 and #404 appeared to have continued to erupt, so 2-3mm removed off crowns bilaterally, then restoration repeated.

This surgery appeared to heal completely.

10 months later, the ONF had reoccurred - possibly due to:

“Trampoline effect” due to loss of underlying supporting bone putting stress on the soft tissue over the palate.

Owner was found to be feeding daily chicken carcasses as breeder’s recommendation, (against veterinary advice).

Dog may be using lower canine #404 quite heavily and stressing the area by breaking the food between tooth and hard palate.

Same effect but incisors (#403) involved rather than canine. Slight dimple allowed food and debris to collect- creating palatitis leading the break down of

the area Infection/ inflammation in nasal passage leading to break down from other side Unidentified issue / incomplete healing firm previous flap repair.

4th treatment (2 years 2 months of age)

Procedures performed: GA. Auricular cartilage harvest, sutured into ONF.

1 week later, the repair had broken down- possibly due to:

Continued chewing and use of tooth. Owner had another dog (young puppy) at home with who he plays rough.

Poor suturing of flap into position. Incomplete preparation of ONF Infection at site. Too much debris accumulating at site causing inflammation and pressure Interference from another tooth other than canine #404

5th treatment (2 years, 2 months and 2 weeks of age)

Procedures performed: GA. Sliding palatal flap. Extraction of #402 and #403. Orthodontic device (figure 8 wire bonded across #104 and #204) placed, then removed shortly post op as dog broke this device.

1 week later, this repair was found to have partially broken down in rostral section, possibly due to:

Continued interference from dog due to chewing habits. Organic debris (grass seeds) in wound site.

6th treatment (2 years, 2 months and 3 weeks of age)

Procedures performed: GA. Cleaning of site and further placement of sutures.

2 weeks later, the site appeared to be healing well.

4 weeks later, the site appeared to have almost completely finished healing.

Limitations:

In this case, there are a number of difficulties:

Dog behaviour- both vet and client were unable to examine palate without general anaesthetic (GA)- even being unable to open his mouth without heavy sedation! This means we are unable to clean the wound site at home, carefully monitor it, and unable remove accumulated debris. Also, it made the use of a palatal obturator impossible, as this would involve a compliant animal to remove and replace the device.

Repeated failures meant further loss of bone to the hard palate. Repeated repairs had resulted in scar tissue on the hard palate, meaning each subsequent

repair needs to be more aggressive. Initially, it was thought that the mandibular canines had erupted asymmetrically- eruption of

#304 had been truncated because of its contact with the palate whereas #404 had continued to erupt and was responsible for the complete penetration of the palate. However, a mild wry bite was not identified until late in the case, so this may explain the asymmetry of the canines/ ONF, and also it could be possible that the right lower incisors may have contributed to the ONF.

The dog’s oral inclination- will chew on anything it can find (other dogs, vegetation, fabric/ bedding etc). It also bites down very hard/ aggressively- as shown by the quick breakage of the orthodontic appliance fitted (the reinforced figure-8 wire).

Other options for repair:

Extract 103, and raise a large mucogingival flap.    

 

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Rhinolithiasis in Humans and Companion Animals – A Literature Review

Dr Kevin Ng

Perth Pet Dentistry

PO Box 1080

Roleystone WA 6111

Introduction

Rhinoliths are formed from the precipitation of mineral salts around a nidus in the nasal cavity. They are extremely rare. Over a 17-year period between 1988 and 2005, only 28 cases were reported in the human literature (Orhan et al. 2006). In comparison, only 2 cases of rhinolithiasis have been reported in the veterinary literature, both in dogs (Schuenemann & Oechtering 2012). They are classified according to the origin on the nidus around which they are formed, stones arising around foreign material are termed exogenous, whereas those arising around material of organic origin from the patient are termed endogenous (Polson, 1943).

Pathogenesis

Many items may act as a potential nidus. Exogenous nidi reported in humans include seeds, beads, buttons and pebbles (Barros et al, 2005 and others). Iatrogenically introduced materials such as cotton wool and swabs have also been reported. Endogenous nidi are much more uncommon, with the prevalence of exogenous to endogenous nidi estimated to be around 7:1 (Polson, 1943). In companion animals, plant material has been identified as the offending nidus in one dog (Schuenemann & Oechtering, 2012). Once in situ, the nidus acts as a kernel for the precipitation of mineral salts. This occurs despite normal serum calcium and phosphorous levels (White & Pharoah 2014). While normal nasal and lacrimal secretions may be involved, these mineral salts are mostly derived from chronic inflammatory secretions associated with the offending nidus (Bayram et al, 2011). Development of a rhinolith may take years (Polson, 1943). This, and the reduced rate of self-introduced nasal foreign bodies in companion animals, may explain why there have been few reports of rhinolithiasis in the veterinary literature to date.

The nasal obstruction caused by the enlarging rhinolith is believed to contribute to precipitation of mineral salts by preventing the outflow of secretions and altering nasal airflow (Brehmer & Riemann, 2010; Orhan et al, 2006). This may predispose smaller, brachycephalic breeds to developing rhinoliths (Schuenemann & Oechtering, 2012).

Clinical Signs

Clinical signs are associated with inflammation and nasal obstruction secondary to the presence the rhinolith. In humans, these typically include nasal obstruction, discharge, epistaxis, facial swelling, epiphora, pyrexia and pain (Appleton et al, 1988, and others). Clinical signs reported in 2 dogs included chronic nasal obstruction, nasal discharge and dyspnoea (Schuenemann & Oechtering, 2012). However, clinical signs are not present in all cases and rhinoliths have been reported as incidental findings on imaging studies of the head and oral cavity during workup for other conditions (Appleton et al, 1988 and others).

In chronic cases, erosion of the nasal or maxillary septum, sequestrum formation, palatal perforation and sinusitis have been reported (Orhan et al, 2006; Pinto et al, 2007). Nasal septum deviation has been reported in a dog (Schuenemann & Oechtering, 2012).

Diagnosis

Rhinoscopy, intraoral radiography or CT imaging can be used for the diagnosis of rhinolithiasis. Of these, CT imaging may be the most sensitive due to its ability to detect small amounts of calcium, and lack of anatomical superimposition (Orthan et al, 2006). CT imaging also has the added benefits of being able to more accurately determine the exact location, size and shape of the rhinolith, as well as being able to identify potential complications such as palatal or septal perforation (Bayram et al, 2005).

Endoscopy is a useful adjunct to CT and has the added benefit of being minimally invasive, as well as potentially allowing rhinoscopic removal of the rhinolith and biopsy to rule out other conditions.

An understanding of the appearance of rhinoliths on intraoral radiography is important, as dentists have frequently been the first to identify cases (Appleton et al, 1998, and others). These cases are typically asymptomatic and intraoral radiographs were being performed to evaluate oral disease. In cases where nasal disease is being investigated, intraoral radiography should not be used to rule out rhinolithiasis as incompletely calcified stones may not show up on routine films. If rhinolithiasis is confirmed on intraoral radiography and no other diagnostic options are available, multiple views from different projections should be performed to provide as much information regarding size, shape and location as possible (Barros et al, 2005).

On intraoral radiographs, rhinoliths are typically radiopaque objects of with a well-defined border (White & Pharoah, 2014). Radiopacity is variable and may be either homogenous or heterogenous, occasionally with an area of central lucency or annular characteristics (White

& Pharoah, 2014). The radiographic outline is variable, but is usually irregular (Appleton et al, 1988).

Confirmation of rhinolithiasis can be achieved by submission of the stone for analysis. They typically consist of around 90% inorganic and 10% organic material (Brehmer & Riemann, 2010). The inorganic components usually include varying amounts of calcium phosphate, magnesium phosphate and calcium carbonate (Appleton et al, 1998; Polson et al, 1943). Other components reported in smaller amounts in the human literature include magnesium carbonate, calcium stearate, oxalate, fluoride and iron (Appleton et al, 1998, and others). Stone analysis has only been reported once in the veterinary literature. A stone consisting completely of calcium carbonate was retrieved from a dog (Schuenemann & Oechtering, 2012). Sectioning of a rhinolith may reveal the offending nidus, although they are not always apparent.

Histopathology of any abnormal tissue is recommended to rule out neoplastic conditions. It may also be helpful in identifying nidi that are not evident on gross examination (Schuenemann & Oechtering, 2012).

Differential Diagnoses

Differentials for radiopaque objects within the nasal cavity include radiopaque foreign bodies, retained roots, impacted teeth, sequestra, and calcified neoplasms such as odontomas and chrondrosarcomas (Barros et al, 2005).

Treatment

The treatment of choice in humans is endoscopically guided removal (Barros et al, 2005 and others). Larger rhinoliths may be fragmented into smaller pieces prior to removal (Bayram et al, 2011, and others). A variety of surgical approaches for the removal of rhinoliths in humans have been described. Methods of rhinolith removal reported in companion animals include endoscopic removal and laser-assisted turbinectomy (Schuenemann & Oechtering, 2012). The more invasive approach in the latter case was required due to complications arising from chronic rhinitis and previous surgical attempts at treatment. If endoscopic removal is not successful, then more invasive approaches to the nasal cavity may be required. Ventral, dorsal and lateral approaches to the nasal cavity have previously been reported (Hedlund, 1998). An approach to the rostral nasal cavity through the alveolar mucosa has also been described in dogs (Priddy et al, 2001). Haemorrhage should always be considered as a potential complication

Conclusion

Even though rhinoliths are extremely rare in companion animals, as the use of intraoral radiography becomes more prevalent, it is possible that an increased number of cases may be diagnosed, especially those that are asymptomatic. Therefore, knowledge of the radiographic appearance on dental radiographs and potential differential diagnoses is vital. Rhinoliths should also be considered as a rare differential diagnosis in cases with chronic nasal obstruction and/or discharge.

References

Appleton SS, Kimbrough RE, Engstrom HIM, Rhinolithiasis: a review. Oral Surg Oral Med Oral Pathol 1988; 65:693-698.

Barros CA, Martins RR, Silva JB, et al. Rhinolith: a radiographic finding in a dental clinic. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 100:486-490.

Bayram B, Deniz K, Ozsoy OP, Uckan S. A simple surgical approach for management of the rhinoliths: case report. J Oral Maxillofac Surg 2011; 69:1403-1407.

Brehmer D, Riemann R. The rhinolith – a possible differential diagnosis of a unilateral nasal obstruction. Case Reports in Medicine 2010 4. Article ID 845671.

Hedlund CS. Nasal cavity. In: Bojrab MJ, Ellison GW, Slocum B, eds. Current Techniques in Small Animal Surgery. 4th ed. Baltimore: Williams & Wilkins, 1998:343–56.

Orhan K, Kocyigit D, Kisnisci R, Paksoy CS. Rhinolithiasis: an uncommon entity of the nasal cavity. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006; 101:E28-E32.

Pinto LSS, Campagnoli EB, Azevedo RS, et al. Rhinoliths causing palatal perforation: case report and literature review. Oral Surg Oral med Oral Pathol Oral Radiol Endod 2007; 104:E42-E46.

Polson CJ. On rhinoliths. J Laryngol Otol 1943; 58:79-116.

Priddy NH, Pope ER, Cohn LA, Constantinescu GM. Alveolar mucosal approach to the canine nasal cavity. J Am Anim Hosp Assoc 2001; 37:179-182.

Schuenemann R, Oechtering G. Rhinolithiasis in two miniature dogs. Journal of Small Animal Practice 2012; 53:361-364.

White SC, Pharoah MJ eds. Oral Radiology Principles and Interpretation. 2014. Mosby. St. Louis, Missouri.

   

Introducing Endodontics into a General Practice – a case study

Amanda Hulands-Nave BVSc (Hons) MVSt MACVSc (SA Med) MANZCVS (SA Dent)

Bellarine Veterinary Practice, Geelong, Victoria

This paper chronicles the introduction of endodontic procedures into the repertoire of a general veterinary practice in regional Victoria as an example of how other general practices may be able to expand their services by offering advanced dental procedures that can provide an alternative to extraction.

Introduction of any change into an organisation requires planning and repetition. A need for change needs to be established and endodontic therapy clearly makes the claim on the basis of doing the best thing for the pet. Retention of teeth, especially the structural teeth of the head (canines and carnassials) help to maintain the jaw structure. Removal of these teeth is associated with removal of a reasonable amount of bone. Post operative recovery from root canal therapy is very simple as the procedure is relatively painless compared with extractions.

Endodontic therapy was introduced into Bellarine Veterinary Practice in 2012 by a process of NAGGING.

• N – Nominate a Dental “Champion”

• A – Advocate for procedures

• G – Gear up / Skill up

• G – Guarantee

• I - Identify cases

• N – Nurses

• G – Great fun / Rewarding

Nominate a Dental “Champion”

Any change requires a critical mass to change habits and create momentum. A staff member who is passionate about dentistry should be nominated to drive a program to make sure that dentistry and endodontics are at the forefront of staff’s minds constantly so that every patient is assessed for dental disease. Having a thorough dental surveillance program will ensure that teeth that are candidates for endodontic treatment are not missed. Having a dental program that has a heavy emphasis on home care and periodontal prevention, will also help to ensure that more teeth that are found to be endodontically compromised are not concurrently affected by periodontal disease which may affect successful endodontic treatment. Having a thorough dental program will ensure that more teeth come across your operating table and by pure numbers you will find more teeth that are endodontic treatment candidates.

Advocate for procedures

The dental champion’s role is to provide education to fellow staff and clients and constantly remind others when endodontics may be useful. Helping other staff to diagnose potential cases is essential.

Diagnostic algorithms are useful. Establishing a good set of client information handouts and automated pricing estimates will help to facilitate prompt and informative discussion with clients. Many clients are anxious of the need to extract otherwise healthy fractured teeth and are often relieved that this can be addressed locally rather than a trip to a metropolitan centre than can be an hour or more away.

Gear up / Skill up

Before embarking on endodontic therapy it is imperative to learn how to do the procedures properly. This can be done via short courses and /or spending time with another veterinary dentist and following up with practice on cadaver heads or extracted teeth. Investment in quality equipment is also essential. In general practice time efficiency is a high priority as caseloads across the range of services (not just dental) are generally higher than specialist practices. Consideration should be given to rotary endodontic equipment which increase speed and also provide a more consistent result. The initial setup costs are greater, but gains are made quickly by increased speed. Developing written protocols, cheat sheets and organising materials will help streamline the multi-step procedures and allow different nurses to be able to assist you if your regular nurse is not available or working in a different part of the practice. Developing endodontic skills can differentiate your practice from your other general practice competitors.

Guarantee

It may be helpful when starting out to offer a guarantee of your endodontic work for a number of cases in order to increase your case experience. This helps to provide some assurance to clients when your experience is minimal. We offered a guarantee for the first 10 cases that if the endodontic treatment failed then we would extract the tooth at no charge. This helps the owner to feel that they have at least given the tooth a chance to be saved and if it does not work they are not at a financial loss. Some clients may choose to opt for extraction immediately to avoid any followup or subsequent procedures and it all comes down to individual risk assessment. At our practice we had no cases that needed to claim that guarantee. Providing the guarantee should be only used as a safety net and not as an excuse for substandard skills and experimentation.

Identify cases

Choose your cases wisely. Select them for a high chance of success, especially in the early cases. Avoid cases with severe periodontal disease, root resorption, tooth root abscesses etc. Once techniques are honed, some of these more borderline cases may be attempted in more complex treatments but in the early days these cases are better referred. It is essential in general practice to attempt the cases that provide “easy wins”.

Nurses

Nurses are essential for perpetuating the momentum from the dental champion and in our practice perform a lot of out patient dental monitoring and home care prevention. Their eyes are often the first to identify teeth that may be endodontic candidates. Nurses are also great advocates for the patients and so education about the benefits of saving teeth will translate into them advocating for endodontic treatment to be considered by the owner initially and then the vet can follow up. This double approach often results in a higher percentage of owner compliance with recommendations.

Great fun / Rewarding

Saving teeth and learning new skills improves job satisfaction which helps to increase enthusiasm and further contributes to the momentum and the cycle begins again.

The Properties of MTA and how it can be Manipulated in the Veterinary Environment

Dr William Ha BDSc, GCRC, PhD student (University of Queensland)

School of Dentistry, The University of Queensland Oral Health Centre

288 Herston Road Herston QLD 4006

For copies of slides or further information, please email w.ha@uq.edu.au

Part 1: MTA chemistry and brands

Calcium hydroxide (Ca(OH)2) & MTA

Ca(OH)2 paste is the gold standard of endodontic antibacterial medication. Its main antibacterial effect relates to its pH. It takes 7 days for Ca(OH)2 paste, at pH 12, for the surrounding dentin to reach a pH of 9, where bacterial growth in teeth is inhibited.1

Ideal Properties Ca(OH)2 paste Ca(OH)2 cement MTA Brands Calcipup, Pulpdent, Calyxl Dycal, Angelus

Fillapex, Life ProRoot MTA, MTA Angelus

Key / Majority Reactants:

As below Butylene glycol disalicylate(l) + Ca(OH)2(s)

2(CaO)3(SiO2) (s) + 2(CaO)2(SiO2) (s) +12H2O(l)

Key / Majority Products:

Ca+(aq) + 2OH-

(aq) + Gel-like thickening agent (eg Methylcellulose)

Calcium disalicylate(S) + 2H2O(l)

2[(CaO)3(SiO2)2•4H2O](s) + 4Ca+

(aq) + 8OH-(aq)

State & Handling Paste Thick paste that solidifies into flaky cement

Hard paste that solidifies into rock like cement

Immediate pH: 12.5 9-10 12.5 Antibacterial effect

Strong Mild Strong

Long term state: Soluble Semi Soluble Insoluble Promotes healing ✔✔✔ ✔ ✔✔✔ Seals the tooth ✖✖✖ ✖ ✔✔✔ Clinical Indication Therapeutic Dressing Liner Permanent Restoration

Ca(OH)2 resin-cements do not release Ca(OH)2,2 they consume it. They contain Ca(OH)2 in their formulation, however, in their setting reaction, Ca(OH)2 is consumed in resinous cement. Their pH is therefore less than the other Ca(OH)2 mediums which do not consume Ca(OH)2 in the setting reaction. 3

Mineral trioxide aggregate (MTA) and procedures

MTA is not a resin cement. It is Portland cement (PC) (calcium silicate) cement that reacts with water to produce Ca(OH)2 as its byproduct and therefore is a setting cement that has the same pH as Ca(OH)2.4 MTA contains 20% Bi2O3 (w/w) to establish radiopacity as set Portland cement alone is indistinguishable from dentine.5 Over a period of several months, the pH of the tooth next to MTA progressively drop in alkalinity.6 In humans, MTAs success rates are 97.6% in pulp capping, 79% in

pulpotomy in permanent teeth and >95% in pulpotomies.7 In apical barriers the success rate can be expected to be over 90%.8

MTA pulp capping

Pulp capping is performed for exposures of the pulp where the pulp itself is not expected to be irreversibly inflamed and currently vital. Aseptic technique is mandatory and any burs used on the tooth should be water-cooled to prevent over heating of the pulp. Once the pulp is exposed using handpieces, haemostasis of the pulp should be achieved via sterile cotton pellet soaked in saline. If haemostasis cannot be achieved it is likely that the area of the pulp is inflamed and you should consider extending your preparation until all inflamed areas of the pulp are removed. Therefore, extend the preparation to a pulpotomy or a pulpectomy. And then place MTA or Ca(OH)2.

Ca(OH)2 has been the gold standard for pulp capping, however, it has problems. Ca(OH)2 is soluble in oral fluids and therefore it can provide an area for bacterial growth once it dissolves. It does not adhere to the tooth and easily dislodges after placement. Instead of Ca(OH)2, MTA can be placed. After placing MTA into pulpal area, place a layer resin-modified glass ionomer cement (RMGIC) over MTA to protect from washing out. Etch the tooth and then wash out the etch. Place prime and bond adhesive and follow with a composite resin restoration.

Discussed in more detail in Accorinte.9

MTA pulpotomy

Pulpotomies are performed for deep carious exposures or exposures of the pulp where the pulp is not expected to irreversibly inflamed and currently vital. The clinical procedure is otherwise the same as a pulp cap with the key difference being the removal of the pulpal chamber.

Much of the above was taken from Barrieshi.10

MTA apexification and apical barrier

The larger the apex the greater the chance that the apical region of the tooth will be inadequately obturated and the more difficult it is for the clinician to length control the obturation material. In the past, multiple appointments to dress the canals with Ca(OH)2 were utilized With MTA, this can be done in one visit.

As MTA is antibacterial, sets hard, and promotes bony growth, clinicians can place MTA at the apex with good confidence the tooth is better obturated than if gutta percha (GP) was placed. Teeth with apices wider than a 55 K-file (0.55mm), and/or when apical patency becomes difficult to achieve, the clinician can consider using MTA instead of GP. Place at least 3-5mm thickness of MTA and then restore the rest with GP, resin, or, more MTA.11

MTA apicoectomy Apical infections that do not respond to conventional and adequate root canal therapy can respond to apicoectomy. This is where the last 3mm of the tooth is removed along with any apical infection and the end of the root canal is sealed with MTA. MTA is used because it has excellent sealing properties and will encourage healing of the bone around it, unlike the historical alternative of amalgam.

Differences between MTA brands

ProRoot MTA MTA Angelus Biodentine MTA Fillapex TheraCal LC What is it really?

PC + Bi2O3 PC + Bi2O3 Modified PC + ZrO

Dycal + PC Flowable resin + PC

Clinical Uses

Endodontic repair + Pulp therapy

Endodontic repair + Pulp therapy

Endodontic repair + Pulp therapy

Sealer Pulp caps only

Packaging 1 use only sachets

Re-sealable jar

Manually combined, capsule mixed

Two part mixing paste syringe

Single one component syringe

Advertised setting time*

4 hours* 15 Minutes* 6 Minutes 2 hours (but needs water from dentine)

Light Cured

Evidence base

Very extensive studies. Very successful

Extensive studies. Comparable to ProRoot

Mostly small trials. Promising results

Performance ≤ AH26

Mainly anecdotal and lab studies

Cost to buy

2 grams (4 sachets) $350

1gram jars for $100.79

15 capsules $193.50

12g for $165 $36 for 1gm.

Cost per use

$85/use or $25/use (re-using contents)

$14.40/use $12.90/use $16.50/use $1.21/use

Supplier Dentsply Gunz Halas Gunz Erskine Dental & Amalgadent

ProRoot MTA ProRoot MTA is provided as sachets are intended to be one-use only, however, many clinicians opt to use the sachets multiple times to save on cost-per-use. This is, however, against the manufacturer’s instructions. Their advertised setting time of 4 hours is based on a test to resist indentation by 5MPa.12 However, clinicians can carefully place other restorative materials above MTA after 10 minutes as the MTA has reached sufficient hardening.13

MTA Angelus

MTA Angelus comes in a re-sealable jar, which is easier to store for re-use than ProRoot. Its advertised setting time of 15 minutes is based on a test to resist indentation by 0.3MPa.12 Therefore it’s frivolous to compare it with ProRoot MTA based on advertised setting time. Biodentine Biodentine is provided with powder in a capsule with an aqueous solution must be poured into the capsule prior to mixing. It does in fact set faster than the other MTAs, however, it is not hard enough to be a conventional restorative material, such as glass ionomer cement (GIC). MTA Fillapex MTA Fillapex is essentially dycal mixed with MTA powder. It is a flowable endodontic sealer and should not be used for endodontic repairs of teeth or for pulp therapy. It requires water to diffuse from

the dentine to set the sealer and therefore the setting time is uncertain. Furthermore, it higher solubility and greater cytotoxicity than other endodontic sealers (such as AH Plus) and therefore the long-term seal of the tooth can be inferior.14-17 TheraCal LC TheraCal LC has been reported, and marketed, as having high calcium ion release and as being able to create an alkaline pH,18, 19 however the assays used involved placing the material into water and measuring changes over only a few days. TheraCal is not mixed with water on placement and therefore it cannot be expected to perform as such, in vivo. Compared to Vitrebond and Ultrablend Plus, TheraCal LC has less cytotoxicity, however, it has not yet been compared to MTA.20

Part 2: Handling MTA

Clinical Environment

Acid and MTA The setting of MTA features alkaline reagents and products which can be attacked by acids resulting in changes in final structure, greater leakage and less adhesion to tooth structure.9,10 Endodontic infections will create an acidic environment which would degrade the MTA. To neutralize the acid environment, dressing the canal with Ca(OH)2 for 1–2 weeks before MTA placement will improve the properties of the set MTA.12 If placement of Ca(OH)2 is not feasible, substantial irrigation of NaOCl is recommended to neutralize the acid. 21

Ca(OH)2 dressings can also impair the properties of MTA as the various additives, such as methylcellulose and carboxymethylcellulose, can retard the setting of the PC in MTA.16,17 Therefore, if a dressing of Ca(OH)2 paste is used, extensive irrigation should be carried out to ensure that no remaining dressing material is present, as remnants of the cellulose thickener will retard the setting of MTA.21

EDTA, etch and tooth conditioners must be adequately washed away before MTA placement.21 NaOCl irrigants have pH values above 11 and will neutralize any remaining acids when used to rinse canals.18

Fluid contamination MTA, when set in the presence of blood, will have reduced compressive strength, reduced micro-hardness and less resistance to displacement.29-31 Hemorrhagic contamination should be minimized as it impairs the quality of the set MTA.21

Mixing and curing MTA Mixing time and working time As MTA is mixed, water starts to evaporate from the reacting mass as well as being consumed by the setting MTA. Therefore, the workability dramatically changes in a short amount of time. MTA’s working time is 6 minutes.22 A trick to extend the working time is to cover the MTA with wet gauze so less water will evaporate from the setting MTA. Mixing tricks The instructions for use state 3 parts power, to 1 part water, by mass. After mixing, if the work time has elapsed, extra water can be added to make the MTA workable again. MTA can be mixed on a glass slab or paper mixing pad, however, paper mixing pads are flimsy and it’s easy to spill the MTA.

To adjust the wetness of the MTA, two cotton rolls can be kept at hand, one dry and one wet. If the mix is dry, squeeze the cotton roll and it will release gently water into the MTA. Ideally, use a Pasteur pipette. If a mixture is too wet, a cotton roll can be used to dab the MTA which will suck up the excess water. The ideal mixture can have amounts lifted with the flat plastic in one whole piece without dripping or crumbling off the instrument. Alternative mixing solutions MTA should be mixed with sterile or distilled water. In the absence of water, local anaesthetic can be used, however, the reaction is lower and the set material is weaker.35,36 NaOCl solution will accelerate the setting reaction of MTA, however, it will result in a weaker compressive strength.35,37 Chlorhexidine gluconate, as a mixing solution for MTA, should not be used as it completely inhibits the setting reaction of MTA.37

Placing MTA MTA Carriers Amalgam carriers and normal hand instruments can be used for large restorations. Damp cotton pellets held by tweezers seem easier to use than traditional packers for compacting MTA. For smaller restorations, MTA carriers can be used. Examples include MAP MTA Carrier, MTA Carrier, and the Dovgan carrier. If excess mixed MTA is left within a carrier after the appointment, the tip may become clogged and seemingly unusable. If this occurs, submerge the carrier in vinegar and use sharp-tipped instruments such as probes and K files to scratch the MTA out from the carrier. Lee block (Also known as, “MTA Pellet Forming Block”) Many clinicians like to insert their MTA as blocks or pillars into a defect. A simple way to shape your MTA into these ideal pillars is to use a “Lee Block”.23 This is a plastic block that has had bur sized grooves. Freshly mixed MTA is placed into these grooves and then pillars of MTA can be lifted out from the base of the groove using a half hollenback or spoon excavator. The pillars can then be inserted into the tooth. This can be bought or self-made using a fissure bur. If several grooves are made and loaded with mixed MTA the clinician can quickly insert several pillars into the tooth without having to stop to insert more MTA into the block. Compacting MTA down a canal Some clinicians like to utilize ultrasonics to compress the MTA with the intent to compact the MTA.24 However, the collisional vibrations on the setting structure of MTA can disrupt the setting structure, reducing micro-hardness and create porosities if ultrasonics are applied for over 2 seconds.25 Removing MTA from tooth walls MTA can be removed from tooth walls using gentle brushing using cotton pellets, micro-brushes, gentle irrigation with water or using irrigation via ultrasonics. Another method is to twist a K file through a cotton roll, which will turn the K file into a long absorbent brush. Curing MTA Much of the historic literature on MTA utilizes a method where a damp pellet is placed above the MTA to protect the material as it slowly set. However, temporizing a tooth with cotton pellets delays completion of the restoration and can compromise the quality of the seal.39 It is now common to gently place GIC, RMGIC or even resin bonding agents onto MTA. Once these materials have set, the clinician can permanently restore the tooth.

Part 3: How to make MTA (for research purposes) and store MTA

APVMA and the “Front Page effect” It is commonly quoted that MTA is, “just overpriced concrete”. However, clinicians should be wary about simple comparisons as it implies that industrial concrete can be used in teeth. In Australia, veterinary chemicals that are supplied for use in the prevention and treatment of animal diseases must be registered by the APVMA. Furthermore, whether something is therapeutic or not, does not

protect it from sensationalised in the media. If a clinician is reported on the news performing operative procedures using ‘every day products’ their reputation in the community can be ruined, even the operative procedure is commonplace or safe. Evidence for industrial PC in teeth There are studies in animals and people illustrating comparative results between MTA and PC.26, 27 Despite these studies finding that PC can be used in dentistry, regulation will never allow an industrial product to be used in medicine as quality assurance in industry is for industrial purposes, not for medical purposes. Furthermore, PC is not radiopaque and therefore fails radiopacity standards for dental restorative materials. Bismuth oxide, Staining & MTA NaOCl will react with bismuth oxide to produce a dark brown precipitate. Therefore, if MTA is used in aesthetically important areas, the tooth should be adequately irrigated with saline to remove NaOCl residue darkening the MTA.22 Regardless of NaOCl use, darkening of the MTA is expected and Ca(OH)2 should be considered if the darkening of MTA is not viewed as acceptable.23 How to make MTA (for research purposes) MTA is made by mixing two powders, 80% PC (w/w) and 20% Bi2O3 (w/w). To achieve a similar level of radiopacity using powders which may not darken as much as Bi2O3, the following percentages of radiopacifiers can be used to replace the 20% Bismuth oxide: 30% ZrO2, 30% ZnO, 30% BaSO4, 10% Au or 10%Ag-Sn alloy.28, 29 The larger the container used to store the powders, the less likely the mixing of the powders will be homogeneous. At present, the largest commercial brand of MTA, MTA Plus (Prevest Denpro Limited, Jammu city, India), is supplied in 8g jars. Storage: Packets vs Jars If sachets of MTA are to be used, they should be used as ‘one-use-only’ as attempts to using remnant powder will result in lower reactivity of the remnant powder as it has partially reacted with water from the ambient humidity.30 If sachets are to be used for multiple cases, it would be prudent to pour the remaining powder into small jars to protect the cement from reacting with ambient humidity. Keeping the sachets within a sterilization pouches is inadvisable as sterilization pouches are designed to enable humidity to pass through the packet. Temperature effects MTA should not be stored in the refrigerator as this will result in reduction in surface hardness, greater porosity and leakage.42,43

References 1. Nerwich A, Figdor D, Messer HH. pH changes in root dentin over a 4-week period following

root canal dressing with calcium hydroxide. Journal of Endodontics 1993;19:302-306. 2. Angelus. MTA Fillapex - Endodontic Sealer - Scientific Profile. URL:

'https://www.clinicalresearchdental.com/marketing/mta fillapex - scientific profile_medium.pdf'. Accessed 16 April 2013.

3. Lombardi T, Di Felice R, Muhlhauser J. Analysis of pH variation of various calcium hydroxide compounds in vitro. Bull Group Int Rech Sci Stomatol et Odontol 1991;34:73-78.

4. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. Journal of Endodontics 1995;21:349-353.

5. Hwang YC, Lee SH, Hwang IN, et al. Chemical composition, radiopacity, and biocompatibility of Portland cement with bismuth oxide. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 2009;107:e96-102.

6. Heward S, Sedgley CM. Effects of intracanal mineral trioxide aggregate and calcium hydroxide during four weeks on pH changes in simulated root surface resorption defects: an in vitro study using matched pairs of human teeth. Journal of Endodontics 2011;37:40-44.

7. Srinivasan V, Waterhouse P, Whitworth J. Mineral trioxide aggregate in paediatric dentistry. International Journal of Paediatric Dentistry 2009;19:34-47.

8. Witherspoon DE, Small JC, Regan JD, Nunn M. Retrospective analysis of open apex teeth obturated with mineral trioxide aggregate. Journal of Endodontics 2008;34:1171-1176.

9. Accorinte Mde L, Holland R, Reis A, et al. Evaluation of mineral trioxide aggregate and calcium hydroxide cement as pulp-capping agents in human teeth. Journal of Endodontics 2008;34:1-6.

10. Barrieshi-Nusair KM, Qudeimat MA. A prospective clinical study of mineral trioxide aggregate for partial pulpotomy in cariously exposed permanent teeth. Journal of Endodontics 2006;32:731-735.

11. Simon S, Rilliard F, Berdal A, Machtou P. The use of mineral trioxide aggregate in one-visit apexification treatment: a prospective study. International Endodontic Journal 2007;40:186-197.

12. Ha WN, Bentz DP, Kahler B, Walsh LJ. D90: The strongest contributor to setting time in MTA and Portland cement. Journal of Endodontics 2015;

13. Tsujimoto M, Tsujimoto Y, Ookubo A, et al. Timing for composite resin placement on mineral trioxide aggregate. Journal of Endodontics 2013;39:1167-1170.

14. Faria-Junior NB, Tanomaru-Filho M, Berbert FL, Guerreiro-Tanomaru JM. Antibiofilm activity, pH and solubility of endodontic sealers. International Endodontic Journal 2013;

15. Waltimo TM, Boiesen J, Eriksen HM, Orstavik D. Clinical performance of 3 endodontic sealers. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 2001;92:89-92.

16. Tavares CO, Bottcher DE, Assmann E, et al. Tissue reactions to a new mineral trioxide aggregate-containing endodontic sealer. Journal of Endodontics 2013;39:653-657.

17. Borges RP, Sousa-Neto MD, Versiani MA, et al. Changes in the surface of four calcium silicate-containing endodontic materials and an epoxy resin-based sealer after a solubility test. International Endodontic Journal 2012;45:419-428.

18. Bisco Inc. TheraCal LC - Resin-Modified Calcium Silicate Pulp Protectant / Liner. URL: 'http://www.bisco.com/catalog/ple_bisco_catitemf.asp?iBrand_Id=156&iCat_Id=28'. Accessed 16 April 2013.

19. Gandolfi MG, Siboni F, Prati C. Chemical-physical properties of TheraCal, a novel light-curable MTA-like material for pulp capping. International Endodontic Journal 2012;45:571-579.

20. Hebling J, Lessa FC, Nogueira I, Carvalho RM, Costa CA. Cytotoxicity of resin-based light-cured liners. American Journal of Dentistry 2009;22:137-142.

21. Ha WN, Kahler B, Walsh LJ. Clinical Manipulation of Mineral Trioxide Aggregate: Lessons from the Construction Industry and Their Relevance to Clinical Practice. Journal of the Canadian Dental Association 2015;81:f4.

22. Wang CW, Chiang TY, Chang HC, Ding SJ. Physicochemical properties and osteogenic activity of radiopaque calcium silicate-gelatin cements. Journal of Materials Science: Materials in Medicine 2014;25:2193-2203.

23. Lee ES. A new mineral trioxide aggregate root-end filling technique. Journal of Endodontics

2000;26:764-765. 24. Yeung P, Liewehr FR, Moon PC. A quantitative comparison of the fill density of MTA

produced by two placement techniques. Journal of Endodontics 2006;32:456-459. 25. Parashos P, Phoon A, Sathorn C. Effect of ultrasonication on physical properties of mineral

trioxide aggregate. Biomed Research International 2014;2014:191984. 26. Sakai VT, Moretti AB, Oliveira TM, et al. Pulpotomy of human primary molars with MTA and

Portland cement: a randomised controlled trial. British Dental Journal 2009;207:E5; discussion 128-129.

27. Silva Neto JD, Schnaider TB, Gragnani A, et al. Portland cement with additives in the repair of furcation perforations in dogs. Acta Cirúrgica Brasileira 2012;27:809-814.

28. Cutajar A, Mallia B, Abela S, Camilleri J. Replacement of radiopacifier in mineral trioxide aggregate; characterization and determination of physical properties. Dental Materials 2011;27:879-891.

29. Camilleri J, Gandolfi MG. Evaluation of the radiopacity of calcium silicate cements containing different radiopacifiers. International Endodontic Journal 2010;43:21-30.

30. Ha WN, Kahler B, Walsh LJ. Particle size changes in unsealed mineral trioxide aggregate powder. Journal of Endodontics 2014;40:423-426.

Dental Materials - Resin Composites  

Wayne Chow – Lieutenant Colonel 

SO1 Dental and Clinical Governance HQ , 17 CSS Bde, Head of Corps , Royal Australian Army Dental 

Corp 

Scope of Presentation 1. Definition 2. Introduction - Resin Composite 3. Chemical Properties 4. Resin Polymerisation Process 5. Classification 6. Current Products – Resin Composite materials 7. Bonding of Resin Composite 8. Current Products – Bonding agents 9. Clinical Considerations 10. Clinical Indications 11. References Definition Composite: (Noun) A thing made up of several parts of elements (Collins Dictionary) Composite: (Noun) Made up of several parts of elements (Oxford Dictionary) Composite Materials: (Noun) Materials made from two or more constituent materials with significantly different physical or chemical properties, that when combined, produce a material with characteristics different from the individual components. (Engineering Magazine April 2007)

Introduction - Resin Composite Resin Composite is a restorative material used in modern Dentistry. It is a tooth coloured dental restorative material. Resin Composite is commonly referred to as ‘white’ filling material often used to replace missing dental hard tissues (Teeth). It is composed of filler particles in a ‘sea’ of resin matrix. Resin adheres to the surface of filler particles by a chemical called Coupling Agents Desired physical properties for clinical use in Dentistry 1. Linear co-efficient of thermal expansion 2. Water Absorption 3. Wear resistance 4. Smooth surface texture 5. Radio-opacity 6. High modulus of elasticity 7. Low solubility

Resin Monomer is a single molecule. Resin Monomers are joined together to form a long chain of monomers called Polymers. This polymerisation process can be initiated by various activation systems using heat, chemical and photo-chemical catalysts. This polymerisation process is often referred to as Curing.

Physical properties of the material are improved by 1. Cross linking of long chains of polymers together improve the physical strength 2. Combining more than one type of monomer to form copolymer also improve the physical strength (Rawls 2003)

Chemical Properties 1. Resin Matrix The base for resin matrix is BIS-GMA.

BIS-GMA bisphenol glycidylmethacrylate Developed in 1950's, bisphenol A was mixed with and glycidylmethacrylate thinned with TEGDMA to form the first generation BIS-GMA resin.

Diluents are added to increase material flow and handling characteristics:

MMA methylmethacrylate BIS-DMA bisphenol dimethacrylate UDMA urethane dimethacrylate

Other diluents are also added to encourage cross linking for improved strength.

TEGDMA triethylene glycol dimethacrylate EGDMA ethylene glycol dimethacrylate

2. Filler Particles

Filler particles are added to the resin matrix to reduce polymerisation shrinkage during the curing process Filler particles may include materials such as

Glass particles – strontium , barium, borosilicate, quartz, silica, ceramic Pre-polymerised resin

Physical properties of the material are generally improved by the addition of filler particles. However material properties can be modified by:

The type of fillers material Surface area, size, shape, surface modifiers, optical index, filler load and size distribution. Filler particles are radio-opaque to contrast dental tissues

3. Coupling Agents

Often referred to as Silane, Silanating agents or Silanating Coupling Agents. They are used to improve adherence of resin to filler particle surfaces. Coupling agents chemically coat filler surfaces and increase the overall strength of the material. They are used for over fifty years in industrial plastics and later in dental materials. Today, they are still state of the art. Common used Silanes include Methacryloxypropyltrimethoxysilane (γ-MPTS)

Silanes used in dentistry do have clinically relevant problems: 1. They age quickly in a bottle and become chemically ineffective 2. Need to check expiry dates 3. They are sensitive to water 4. The bond between Silane-Filler particles will break down with moisture 5. Water absorbed by resin composite material will result in hydrolysis of the silane bond and

eventual filler loss.

Resin Polymerisation Process

Polymerisation of resin is the conversion of monomers into polymer in an additional polymerisation reaction, catalysed by free radical intiators. This process starts with: Activation: Chemical initiators breakdown to form free radicals. Chemical intiators include

1. Benzoyl peroxide (heat and chemical activation) 2. Camphoroquinone (visible light activation)

Propagation: free radicals combine with resin monomer molecules. As a result, monomers join at double bonds to form growing chains.

Termination: when the growth process is complete Other Constituents in Resin Composite material include Pigment to provide the colour and Stabilisers or inhibitors are added to avoid spontaneous polymerisation. Stabilisers are also used to control the activation process of initiators and resin mixtures. Hydroquinone is most commonly used stabiliser

Resin Polymerisation can be interfered by 1. Exposure to impurities and eugenol (a constituent in temporary dental material) 2. Exposure to oxygen in the air. This is also known as Oxygen inhibition. And may result in a

weaker physical property on the surface of the dental resin composite restorations

Chemical Properties

Heat Activation

Heat applied to initiators (over 50°c) breaks down its chemical structure to produce free radicals Common heat based initiators are peroxides such as Benzoyl peroxide t-butylperoxide t-cumythydroxyperoxide Monomers may form chains when heat is applied even without initiators

Chemical Activation Activation of Chemical Initiators such as benzoyl peroxides produces free radicals. This is done by mixing a base paste and a catalyst paste for self curing. Older generation Chemical Initiators are not color stable and MAY affect aesthetics of dental appearance. However, modern formulation has improved for clinical use Photo-chemical activation

Photochemical initiators are activated to produce free radicals when exposed to light wavelengths 450 - 475 nm. Common photochemical initiators are: Camphoroquinone (CQ) Acenaphthene quinone Benzyl Peroxide Amines may be added to accelerate polymerisation time

Photo-chemical polymerisation can be accomplished with the following curing light systems: Quartz-Tungsten-Halogen, Plasma Arc Curing and Light Emitting Diode Curing lights need to be calibrated to ensure full conversation of resin during polymerisation: Light intensity and Correct light wavelength

Classification Dental Resin Composite material can be classified by: 1. Polymerisation Process or Curing Process 2. Size of the filler particles it contain Dental Resin Composite material classified by Curing Process 1 Heat cure Resin Composite

Describes heat application to initiate resin polymerisation. Commonly used in laboratories to fabricate dental prosthesis

Not used intra-orally for obvious reasons! 2 Self cure Resin Composite

Describes chemical initiation converting monomers to polymers, causing resin polymerisation Less commonly used in clinical dentistry due to

porosity and bubbles introduced during mixing Limited working time

3 Light cure Resin Composite

Describes photo-chemical initiation causing resin polymerisation Commonly used in clinical dentistry due to:

Long working time and ‘curing or setting on demand’ 4 Dual cure Resin Composite

Describes chemical cure resin materials combined with photo-chemical initiation resulting in either or both processes to cause resin polymerisation Commonly used in clinical dentistry in:

Light restricted environment Polymerisation continues after initial light curing

Dental Resin Composite material classified by Filler size Resin materials are commonly classified according to the sizes of the filler particles. Particle size ranges from nm to μm dimensions. (Taira 1990)

Macro-filled 5 to 30 μm Conventional Larger filler particles Barium or strontium glass particles - More difficult to polish Resin has 75% to 80% by weight of fillers - Mechanically superior resin composite material

Microfilled 40 to 50 nm Smaller particles colloidal silica glass particles - Good surface polish Resin has 30% to 60% by weight of fillers - More polymerisation shrinkage due to higher % resin Mechanically less superior resin composite material

Poorer wear resistance Unsuitable for load bearing situation

Flowable resin composite is a sub-class of microfilled Resin has 30% to 55% by weight of fillers

Lower viscosity Flowability may vary between different products

Clinical use: Better adaptation to the walls of the cavity and preparation walls Liner under conventional resin composite material Unsuitable for load bearing situation (Puetzfeldt 2002)

Hybrid fillers 10-50 μm and 40 nm Mixture of macro and micro sized particles Optimise the surface properties and mechanical properties Good wear resistance during dental function Improved physical properties and acceptable polishability Resin has 75% to 85% by weight of fillers Commonly available resin composite in the 90s. (Ferracane 1999)

Nanofillers 5 to 100 nm The latest version of hybrid fillers Increase the % of fillers by weight with very small filler size using nano technology (Ferracane

1995) Contains 0.005 to 0.01 μm size ‘nano’ particles in the resin Good material strength and wear resistance ‘Possible’ slight improvement in polishability. (Swift 2005)

Packable Resin Composite Condensable resin composite Addition of larger sized particles and fibres Higher viscosity and Less ‘sticky’ (Rawls 2003) Marketed commercially as easier to handle and shape inter-proximally Material flow may be modified by temperature prior to polymerisation. (Brackett 2000) Current Products – Resin Composite Materials

Microfilled 40 to 50 nm Durafill VS (Heraeus Kulzer) Z100 (3M ESPE) Herculite XRV (Kerr) Heliomolar (Ivoclar Vivadent)

Flowable resin composite Ultraseal XT Plus (Ultradent) Herculite Ultra Flow (Kerr) Filtex Supreme XTE Flowable (3M ESPE) Heliomolar Flow (Ivoclar Vivadent)

Packable Resin Composite Filtek P-60 (3M ESPE) Solitare 2 (Heraeus Kulzer) Surefil (Dentsply Caulk) Prodigy Condensable (Kerr) Heliomolar HB (Ivoclar Vivadent)

Hybrid fillers Herculite Ultra (Kerr) Gradia Direct (GC Corp) Z250 (3M ESPE) Prodigy, Synergy (Coltene-Whaledent)

Nanofillers Filtex Supreme XTE Universal (3M ESPE) Premise (Kerr) Venus Diamond (Heraeus Kulzer)

Bonding of Resin Composite

Successful use of Resin Composite materials in clinical dentistry hinges on the following question: How does it ‘stick’ to a tooth?

The material relies on a chemical bonding process to ‘stick’ to dental hard tissues. This chemical bond involves enamel bonding and dentine bonding

Enamel bonding Enamel is a highly mineralised dental tissue. It is a homogenous tissue: 85-92% mineral (Hydro-xyapaptite) 6-12% water by volume

2-3% organic material

Enamel bonding involves the following steps: First, the tooth surface is modified with an acid primer (35% - 50% phosphoric acid – pH < 1.0) Commonly refers to Acid Etching, it creates surface roughness, porosities and also removes contaminates Also increases the surface energy and ‘wettability’ Acid treated enamel surface is coated with a low viscosity resin cement. This forms resin tags of 10 to 20 μm, mechanically locking into the surface irregularities (van Noort 2008) This creates a strong and predictable resin bond, with reported bond strength of 15-25 MPa (Rawls 2003)

Dentine bonding Dentine is a less mineralised dental tissue. It is a hetrogenous composite tissue 45-50% mineral (Hydroxyapaptite) 20-22% water by volume 30-33% organic material

Dentine bonding is a more complex process and requires dentine bonding agent to bridge the interface It is more difficult and technique sensitive due to the fact that dentine has a higher fluid content and lower inorganic content. Furthermore, the presence of smear layer interferes with bonding (layer of dentine chips, bacteria and other debris) The mechanism dentine bonding is the formation of a Hybrid Layer. This layer involves the micromechanical interlocking of resin around dentinal collagen fibrils that have been exposed by demineralization. The thickness of hybrid layer range from 5 μm to 1μm Dentine bonding involves the following steps: 1. Acid etched enamel and dentine surface 2. Rinse off acid thoroughly 3. A network of collagen fibrils mesh is exposed on dentine 4. Dentine surface should not be desiccated to prevent collagen fibrils from collapsing 5. A hydrophilic Primer is applied on the dentine surface 6. Primer will infiltrate the collagen fibrils mesh 7. Primer will also Infiltrate the dentinal tubules 8. The purpose of a primer is to ‘push’ water away from the dentine fibrils as volatile solvent

component of the primer evaporates from drying 9. Primer also has resin monomers which forms a cross-linking polymer network that infiltrates the

collagen fibrils mesh 10. The resin monomer is the key to Dentine bonding. 11. Finally a bonding resin layer (sealer) is applied and light cured to achieve a polymerised resin

layer 12. Primer also has resin monomers which forms a cross-linking polymer network that infiltrates the

collagen fibrils mesh 13. The resin monomer is the key to Dentine bonding. 14. Finally a bonding resin layer (sealer) is applied and light cured to achieve a polymerised resin

layer 15. Resin composite is then over this layer placed as the restorative material

This protocol remains the gold standards in bond strength and is referred in Dentistry as the total etched technique or Three stage dentine bonding or Fourth Generation dentine bonding

Dentine bonding Advancement of dentine bonding chemistry has decreased the number of clinical steps. New products combine the various components into single bottles including: 2 stages dentine bonding 1 stage dentine bonding

The benefits include clinically ease (Tyas 2004), but bond strength of combined system is compromised (van Noort 2008). Combined systmes and all-in-one systems have a tendency to breakdown on application, resulting in poorer resin infiltration and overall bond strength (Burrow 2012)

Current Products – Dentine Bonding agents

Three stage dentine bonding Optibond FL (Kerr) Scotchbond Multi purpose (3M ESPE)

Two stage dentine bonding – combined primer & bond Scotchbond One (3M ESPE) Optibond Solo Plus (Kerr) Excite (Ivoclar Vivadent) Gluma Comfort Bond (Heraeus Kulzer)

Two stage dentine bonding – combined etchant & primer Clearfil SE Bond (Kuraray Dental) Clearfil Liner Bond 2V Bond (Kuraray Dental)

Single stage dentine bonding Prompt-L-Pop (3M ESPE) G-aenial Bond (GC Australia) G-Bond (GC America)

Clinical Considerations

Resin Composite is used extensively in Clinical Dentistry:

1. Excellent aesthetics (tooth coloured) 2. Low thermal conductivity 3. Conserves tooth structure

Micromechanical retention to etched tooth surface Ability to adhere chemically to tooth substrate

4. No issues or concerns with mercury hygiene or galvanism associated with amalgam alloy materials

5. Working time can be controlled during placement Allows amply of time to shape the final restorations

6. High early strength can be achieved 7. The use of resin composite may strengthen tooth structure depending on factors such as the

design of the cavity or restoration preparation 8. Resin composite restorations can also be easily repaired

Whilst Resin Composites do have a role in Clinical Dentistry, they do have limitation in its physical and handling characteristics. In order to better utilise this material in clinical situations, clinicians therefore need to have a sound understanding of the material science and the modes of failure, in its scope of application in dentistry

A review of Resin Composite restorations examined 24 studies. It found: Most frequent type of failure within 5 years of service is fracture of the restoration Most frequent type of failure beyond 5 years of service is secondary caries Other types of failures include marginal defect and discolouration. (Brunthaler 2003)

Another review of Resin Composite restorations found that Resin Composite restorations fail at a rate 2 to 3 times more than metallic alloy restorations after 8 years of observation (Collins 1998)

Other studies have estimated the survival rate of the following restorations after 17 years observation: Large Resin Composite restorations 7.8 years Amalgam 12.8 years Porcelain fused to Metal crowns 14.6 years (Van Neuiwenhuysen 2003)

Judicious use of Resin Composite is required by practitioners due to the following issues: 1. Placement of resin composite is technically demanding 2. Different rate of wear of the resin material against opposing teeth and other restorative materials 3. Leakage of the materials

Technically demanding

Moisture control is very important Location of the restoration in the mouth and surrounding soft tissues and fluid presence Requires multiple steps and application of primer / sealer Resin composite material is ‘sticky’ to gloves and instruments during handling and placement Packing of the material into a cavity can be challenging Wear of the resin material

Wear performance intraorally is very difficult to assess. Resin composite has limited wear resistance compared to enamel, metallic and ceramic materials. (Yip 2004) Wear of resin composite is influenced by the filler percentage and particle size. Heavily filled resin composite experience less wear than flowable composites. (Clelland 2005)

Flowable resin composite has a lower resistance to wear and reduced mechanical properties

Newer generation of resin composite materials has shown higher wear resistance. Nano-filled resin composites have better wear results. This may be related to 1. a decrease in inter-particle space 2. Resin between fillers is protected by adjacent particles 3. Reduced incidence of filler exfoliation during wear (Schultz 2010)

Leakage of the materials Leakage of the materials around cavity margins may cause 1. Post operative sensitivity 2. Secondary caries

3. De-bonding and dislodgement of the restoration

Resin monomers joining together to form polymer chains during polymerisation causes heat and volume reduction. This volume reduction is known as polymerisation shrinkage. The contraction of the resin material causes a gap at the cavity margin and tooth interface, which is a significant clinical problem. The shrinkage of the resin material also causes material stress at the restoration-tooth interface (prior to the material being completely pulled away). Volumetric shrinkage is estimated to be 1.1% to 3%. Other reports shrinkage to be 1.8% to 8.0%. Internal stress in the form of tensile force at the interface is estimated to be 1MPa to 15 MPs (Rawls 2003) Complete polymerisation may not occur at the deeper part of a restoration due to 1. Depth of cure of the curing light 2. Obstruction to full penetration of the curing light 3. Curing light output is not correct 4. Resulting in a lesser degree of conversion of resin polymers at the deeper part of the restoration

Clinical technical to overcome this problem 1. Use of a dual-cure resin composite (light and chemical cure) 2. Incremental filling or layering technique in the placement of the resin material. General rule for

cavity exceeding 2mm in depth

Leakage may also be due to poor bonding in ‘deep’ cavities. Cavity extending beyond the cemento-enamel junction (CEJ) has little or no enamel to provide predictable resin bonding. It merely relies on almost 100% dentine bonding at the external surface of the restoration: 1. High organic content of dentine prevents a strong resin bond 2. Clinical success is significantly reduced in the medium to long term

Dentine substrate near enamel is more mineralized. However, dentine closer to the pulpal vital tissues is less mineralised and is occupied by more dentinal tubules. This result in poorer dentine bonding of resin composite closer to the pulp and often presents as symptomatic post-operative sensitivity. Therefore, careful clinical assessment may require a liner such as Glass Ionomer Cement in the deeper part of the cavity to ensure a reliable seal and bond at the radicular surfaces. (Burrow 2012)

Degradation of Resin in Aqueous environment Resin polymer degradation occurs naturally:

Swelling or absorption of water - Polymer chains pushed apart and affects the strength of the material 1. Hydrolytic degradation occurring at:

resin / tooth interface (adhesive failure) resin matrix / filler particle interface (cohesive failure)

2. Dissolution of the soluble component of the materials 3. Reduced physical properties of the resin material lead to leakage, fracture and ultimate failure of

the restoration

Clinical Indications

Dental Restorative Materials

Restorations are placed directly in the mouth as a plastic material in order to restore missing tooth structure due to trauma, dental caries. Dentists can model and shaped restorative material into the appropriate form before it polymerises and ‘sets’ intraorally Dental Restorative Materials – Case 1 (posterior restoration) Dental Restorative Materials – Case 2 (anterior restoration)

Dental Cements

Used to retain crowns and bridges Used to chemically bond porcelain restorations on tooth surface To bond metallic restorations on teeth To bond indirect cast posts and cores to root canal systems of teeth Dental Cements – Case 3 , 4, 5

Dental Core Material

Used to replace missing tooth structure to provide resistance and retention for crowns and bridges Dental Core Material – Case 5

Occlusal Rehabilitation

Used to replace missing tooth structure due to extensive tooth surface loss (TSL). Causes of TSL include 1. Erosion and diet related causes 2. Erosion and intrinsic causes 3. Abrasion 4. Attrition 5. Combination of the above Occlusal Rehabilitation – Case 6

Reference

1. Brackett W, Covey D. Resistance to condensation of condensable resin composites by a mechanical test. Oper Dent 2000;25:424–6.

2. Brunthaler A, Konig F. Longevity of direct resin composite restorations in posterior teeth. Clin Oral Investig 2003; 7(2):63-70

3. Burrow MF, Tyas MJ. Clinical Investigation of G-Bond resin based adhesive to non-carious cervical lesions over 5 years. Australian Dental Journal 2012; 57(4):458-463

4. Clelland NL, Pagnotto M. Relative wear of flowable and highly filled composite. Journal of Prosthetic Dentistry 2005; 93(2):153-157

5. Collins C, Bryant R. A clinical evaluation of posterior composite resin restorations: 8 year findings. Journal of Dentistry 1998; 26(4):311-317

6. Ferracane JL. Current trends in dental composite. Crit Rev Oral BiolMed 1995; 6(4):302–18. 7. Reference 8. Ferracane JL, Berge HX, Condon JR. Invitro aging of dental composites in water – effect of

degree of conversion, filler volume, and filler/matrix coupling. J Biomed Mater Res 1998; 42(3):465–72.

9. Peumans M et al. Porcelain veneers: a review of the literature. Journal of Dentistry 2000 ; 28:163–177

10. Puetzfeldt A, Asmussen E. Composite restorations: influence of flowable and self-curing resin composite linings on microleakage in vitro. Oper Dent 2002;27(6):569–75.

11. Rawls HR, Upshaw JE. Restorative resins. Anusavice KJ, editor. Phillip’s science of dental materials.11th edition; 2003. p. 399–441.

12. Schultz S. Mechanical Properties and three body wear of dental restoratives and their comparative flowable materials. Quintessence International 2010; 41(1): e1-10

13. Stangel I et al. Adhesion to Tooth Structure Mediated by contemporary bonding systems. Dental Clinics of North America, 2007; 51(3) 677-694

14. Swift EJ. Nano Composites. J Esthet Restor Dent 2005;17:3–4. 15. Taira M,Suzaki H,Wakasa K, et al. Preparation of pure silica glass filler for dental composites by

the sol-gel process. Journal of British Ceramics Transactions 1990;89:203–7. 16. Tyas MJ, Burrow MF. Adhesive Restorative Materials: A Review. Australian Dental Journal 2004;

49(3):112-121 17. Van Noort R. Introduction to Dental Materials. 2008; 3rd Edition Elsevier 18. Van Nieuwenhuysen JP et al. Long-term evaluation of extensive restorations in permanent teeth.

J Dent 2003; 31(6):395-405 19. Yip DH, Smales RJ. Differential wear of teeth and restorative materials: Clinical implications. The

international Journal of Prosthodontics 2004. 17(3): 350-356

A dental perspective on oral tumour management

Dr. Anthony Caiafa BVSc BDSc MANZCVS

North Coast Veterinary Specialists, Tanawha, Sunshine Coast

Lecturer in Veterinary Dentistry

James Cook University, Townsville

Intraoral radiography

Clinicians are aware that no imaging modality is accurate enough to diagnose the extent of oral tumour invasion. In human oral oncology, a combination of imaging modalities is used to assist in formulating a more accurate determination of tumour spread. A combination of intraoral and/or extraoral plain imaging (panoramic or OPG) combined with CT scans improved determination of tumour spread.

In veterinary oral oncology, extraoral plain imaging with or without CT/MRI scans has been the mainstay for diagnosis and management of oral tumours. The use of intraoral imaging has been limited in veterinary oral oncological management mainly due to poor accessibility.

It must be said that all imaging modalities can under or overestimate the extent of oral tumour invasion

Benefits of intraoral radiographs for oral pathology and tumour management

Easy to perform. Size 4 (57mm X 76 mm) or 5 film ideal. May be the only imaging necessary when dealing with benign lesions/cysts/tumours

especially in the rostral maxilla/rostral mandible/body of mandible. There may be no need for more expensive imaging such as CT scan or MRI

Can be combined with plain extraoral imaging to assist in tumour management Assists in diagnosing/ managing nasal pathology (and jaw fractures) Aid in the detection of post-surgical complications such as fractured roots, pulp

necrosis and bony sequestrae

Drawbacks of intraoral radiographs for tumour management

Only 2 dimensional image Soft tissue imaging is relatively poor May not be diagnostic for more caudal tumours, CT is better Requires about 40% mineral loss in bone/tooth to see radiolucency Tumours of soft tissues/tongue better imaged by MRI As with other radiographic imaging modalities- may be difficult to determine spread of

tumour within the mandibular canal

Some dental/oral complications seen following oral tumour resection

Retained tooth roots, damage to teeth and possible pulp necrosis and infection Malocclusions including mandibular drift following surgery: Rostral/body

mandibulectomy caudal to the symphysis, caudal mandibulectomy including ramus and condylar head and total mandibulectomy

TMJ dysfunction Dry mouth and oral disease following irradiation of the head

Prevention/Correction of mandibular drift and hard palate trauma from mandibular canine tooth

Rim excision for benign/early detected malignant tumours** Tooth extraction of maloccluded tooth (teeth) Crown reduction and pulpotomy therapy (requires extra/ intraoral radiography) Odontoplasty (requires extra/ intraoral radiography) Rigid internal fixation preferably with small locking plates to stabilise mandible in

case of rostral/body mandibulectomy +/- use of bone replacement materials Orthodontic brackets/elastic chain^

** Murray R., Aitken M. and Gottfried S. The Use of Rim Excision as a Treatment for Canine Acanthomatous Ameloblastoma. JAAHA, March/April 2010, 46. 91-96

^ Bar-Am Y and Verstraete F. Elastic training for the prevention of mandibular drift following mandibulectomy in dogs; 18 cases (2005-2008) Vet Surg. 2010 Jul; 39(5): 574-580

Reconstructive techniques in human and veterinary oral oncology

Radial/fibula vascular flaps. First performed in 1989. Ability to place implants and crowns to alleviate poor mastication and aesthetics Use of compressive matrix infused with human BMP and locking plates*^^

* Boaz A., Verstraete F., Huey D. Cissell D. and Kyriacos A. Regenerating Mandibular Bone Using rhBMP‐2: Part 1— Immediate Reconstruction of Segmental Mandibulectomies. Vet Surg., Jan., 2014 1-7.

^^ Boudrieau R. Initial Experience With rhBMP‐2 Delivered in a Compressive Resistant Matrix for Mandibular Reconstruction in 5 Dogs Vet Surg., 44, 2015 443-458

Odontogenic tumours

Dr Anthony Caiafa

North Coast Veterinary Specialists, Tanawha, Sunshine Coast

Lecturer in Veterinary Dentistry

James Cook University, Townsville

Odontogenic tumours are unique to the jaws and originate from tissue associated with tooth development. Their incidence has been reported to be about 0.5-0.7% of all tumours in dogs and cats.

An understanding of tooth development will aid in a better appreciation of how these tumours arise.

Odontogenesis

Tooth formation arises from the “budding” of the basal cell layer of the oral epithelium. This basal cell layer penetrates the connective tissue (invagination) and as it does so, it thickens to form a concavity (cap stage). It stays attached to the basal epithelial layer by an elongated cord (dental lamina). The cap structure enlarges and the bottom layer of epithelium (inner enamel epithelium) separates from the top layer (outer enamel epithelium). The zone between these two layers is called the stellate reticulum (early bell stage).

Elongation of the periphery of the epithelial structure leads to the formation of specialised epithelium that induces the adjacent connective tissue to finally form dentine and pulp. This altered connective tissue is called the dental papilla. The outer zone of connective tissue that encapsulates the developing tooth bud is called the dental follicle. The crown portion of the follicle when the tooth erupts becomes part of the connective tissue of the free marginal gingiva and the root portion becomes the periodontal ligament.

In the late bell stage, the cells of the inner enamel epithelium elongate and there is migration of the nucleus away from the basement membrane (reverse polarisation) in each cell (presecretory ameloblasts). Cells in the adjacent dental papilla undergo this reverse polarisation of their nuclei and become presecretory odontoblasts. As the ameloblasts mature, these odontoblasts are stimulated to lay down dentine which in turn initiates the laying down of enamel matrix on the other side of the basement membrane. The dental lamina begins to break up and the islands of cells left behind become the rests of Serres.

As the tooth develops, the epithelium that forms the outer rim of the bell shaped enamel organ elongates forming the roots. This epithelium forms a thin transient membrane called Hertwig root sheath. The odontoblasts opposing this sheath produce the root dentine. Eventually the root sheath breaks up (forming epithelial remnants or the Rests of Malassez) and this allows the newly formed root dentine to come into contact with the connective tissue cells of the dental follicle. The dentine then stimulates these cells to differentiate into cementoblasts and produce cementum. Cementum allows the periodontal ligament to attach to the tooth surface.

Odontogenic tumours are often classified according to their tissue of origin. Therefore, epithelial odontogenic tumours (e.g. ameloblastoma) arise from residual odontogenic epithelium. Connective tissue or mesodermal odontogenic tumours (e.g. peripheral odontogenic fibroma) arise from connective tissue elements and mixed odontogenic tumours contain both epithelium and connective tissue (ectomesoderm) from the stages of odontogenesis (e.g. odontoma).

Odontogenic tumours may also be classified as inductive (e.g. odontoma) with the interaction between epithelial and connective tissue elements to produce enamel, dentine and pulp or non-inductive (e.g. ameloblastoma) where there is no hard tissue formation.

Epulides

The epulides are similar to gingival hyperplasia in appearance and are usually confined to the gingival margin. They are often slow growing, firm, and generally covered by intact epithelium.

They are considered to be odontogenic in origin, arising from dental lamina remnants from odontogenesis (possibly in the periodontal ligament or gingival tissues).

“Benign” masses such as focal fibrous/generalised gingival hyperplasia and the epulides are by far the most common “growths” encountered in the oral cavity of dogs. Focal fibrous hyperplasia (localised gingival hyperplasia) is usually a reactive growth due to a long standing underlying irritant such as plaque/calculus. It is often clinically and histo-pathologically misdiagnosed as an epulis.

The treatment of gingival hyperplasia is by local excision and management of the underlying cause. Epulides tend to be rare in the cat.

There is also a drug induced form of generalised gingival hyperplasia seen in dogs on cyclosporine medication, as well as a familial hyperplastic lesion reported in Boxer dogs.

Many “benign” gingival masses in old dogs go unreported, so that gingival hyperplasia and fibromatous/ossifying epulis are underreported in surgical biopsy specimens. However, in one survey of oral biopsy specimens submitted to a veterinary pathology laboratory, the epulides still made up approx. 36% of samples submitted.

The term epulis is a clinically descriptive term referring to a localised non-specific exophytic growth on the gingiva. Most epulides are benign non-neoplastic lesions, containing remnants of the dental lamina located in the periodontal ligament or gingival epithelium, but an excised epulis should always be submitted for histopathology to determine the true nature of the lesion. Epulides have a predilection for the rostral (anterior) mandible/maxilla and maxillary fourth premolar region, but can occur anywhere on the gingival mucosa.

Epulides contain dental lamina cells from the periodontal ligament or gingival epithelium and are divided into mainly three types, namely fibromatous (fibrous) epulis, ossifying epulis and the locally invasive acanthomatous epulis. A fourth type, namely the pyogenic granuloma is rare, and will not be discussed here.

Fibromatous epulis can be single or multiple and usually has a smooth, pink surface, although it can become erythematous and ulcerated due to occlusal or masticatory forces. If large enough it can cause pain and interfere with mastication. It does not invade bone.

Ossifying epulis is probably of periodontal ligament/gingival epithelium origin. These growths show metaplastic bone formation, and varying amounts of osteoid material can be seen within them. This osteoid material may appear on radiographs. In addition, strands of odontogenic epithelium are often present in varying amounts.

Recently, there has been a reclassification of both Fibromatous and ossifying epulides into the one classification called peripheral odontogenic fibroma.

Peripheral odontogenic fibroma (POF) is best treated by block resection due to the possible origin of the mass from the periodontal ligament surrounding a tooth. This requires extraction of the tooth or teeth associated with the mass.

Acanthomatous epulis (canine acanthomatous ameloblastoma), although classified as benign, can be locally aggressive, displace teeth, invade into bone and is considered the most common invasive tumour of the dog jaw. When 40% or more of the cortex is destroyed, bone lysis may be observed. However, apparently normal radiographs do not rule out bone invasion. If a tumour appears fixed to the underlying bone, then it can generally be assumed that there is microscopic invasion of the bone. Fortunately, acanthomatous epulis does not metastasise and can be controlled by wide local excision including bone. There has been one report of hypercalcemia being associated with this tumour.

Acanthomatous epulis may be referred to as a peripheral ameloblastoma or basal cell carcinoma in some of the veterinary literature. The tumour often consists of sheets and anastomosing bands (palisades) of pleomorphic epithelial cells of odontogenic origin. These cells exhibit reverse polarity of the nuclei similar to ameloblasts. The tumour shows a biologic behaviour similar to intra-osseous ameloblastoma in man and the term Canine Acanthomatous Ameloblastoma (CAA) has now been accepted as best describing this type of tumour.

Current treatment recommendations include aggressive surgical resection, radiation therapy or a combination of the two. Other treatments that have been used with variable success include intralesional anti-cancer drugs (esp. bleomycin) and surgical debulking followed by aggressive ablation with CO2 laser.

At present, radical surgery (up to one cm. margins, based on radiographs or CT) offers the best results with less than 5% recurrence.

Radiation therapy is also effective, but there were reports of malignant tumour transformation at the irradiated site in approximately 20% of cases treated with irradiation. This could develop years after the original tumour removal.

Non- tumour masses include cysts associated with teeth or post pulp necrosis- dentigerous cysts, radicular cysts, and residual cysts.

Ameloblastoma

The ameloblastoma is an uncommon benign neoplasm derived from residual epithelial components of tooth development. In this tumour, the ameloblast-like cells do not induce the connective tissue cells and there is no hard tissue formation.

The ameloblastoma is one of the most common odontogenic tumours (occasionally incorrectly referred to as an adamantinoma). This tumour usually presents as a locally invasive neoplasm with osteolysis around the tooth roots and cystic changes. The classic histological appearance of an

ameloblastoma is a follicular arrangement of ameloblasts and stellate reticulum cells, resembling the basic structure of the enamel organ. Distant metastasis has not been described.

Odontoma

An odontoma is a tumour or more correctly a hamartomatous lesion which contains enamel, dentine, pulp, and cementum in either recognisable tooth shapes (compound) or a solid gnarled mass (complex). Because most occur during the period of normal tooth development and often reach a fixed size, they are not considered true neoplasms, but hamartomas (non-neoplastic developmental masses). They are slow growing, expansile lesions that occur mainly in young animals.

The compound odontoma exhibits advanced cellular differentiation containing mature dental tissues, whereas the complex odontoma has dental hard tissues that bear no resemblance to a tooth. Odontomas have been diagnosed in young dogs, horses and cats.

The radiological appearance is typical and shows an intra-osseous radio dense mass surrounded by a thin radiolucent zone. Compound odontomas are usually unilocular and contain multiple radiopaque structures that resemble miniature teeth (denticles). The number of denticles they contain can vary from a few to many. Complex odontomas appear as a solid radiopaque mass, with a radiolucent band around it.

An odontoma is often associated with an unerupted tooth, a dentigerous cyst, or may be attached to an otherwise normal tooth.

Treatment consists of enucleation and removal from the surrounding bone.

Amyloid-Producing Odontogenic Tumour

This is a rare jaw tumour of cats and dogs. It has been referred to as the veterinary equivalent to the human calcifying epithelial odontogenic tumour (CEOT), although this has been shown to be incorrect. The two tumours are quite different histologically and so the term amyloid-producing odontogenic tumour is now used in the veterinary literature.

These tumours can occur as gingival masses, and is uncertain whether they can also arise from within the bone.

Histologically, the tumour is composed of irregularly shaped strands of squamous epithelium, which in some areas exhibits the palisading of basal cells seen in ameloblastomas. Stellate reticulum may occur and the other prominent feature is the production of the protein, amyloid (enamel matrix), hence the name amyloid-producing tumour.

Recurrence after excision has been reported, although a block resection may be too drastic a surgical procedure for these tumours. Metastasis has not been reported.

Feline Inductive Odontogenic Tumour

This tumour type was originally described in young cats (6 months to 2 years) as an inductive fibroameloblastoma; however it is not a variant form of ameloblastoma. It is a rare tumour in the cat, and contains elements of connective tissue and epithelium, therefore being a mixed odontogenic tumour. It is not well circumscribed, and histologically consists of fibroblastic connective tissue

associated with islands of odontogenic epithelium. Sometimes dentine has begun to form and there may be irregular calcifications associated with the epithelial islands, leading to multiple radiopacities on radiographic examination. There is also varying degrees of bone destruction, production and expansion of the maxilla.

The rostral maxilla is the most common site of occurrence. The tumour may be locally invasive, but metastasis has not been recorded. The tumour requires surgical resection with adequate margins, due to it having indistinct boundaries with surrounding normal tissue. Recurrence is a problem. These tumours may also respond to irradiation.

Biopsy

A “benign” looking gingival mass should have a biopsy performed, so that a diagnosis and treatment plan can be formulated. When multiple oral biopsies are taken, do not confuse biopsy samples by placing all the samples in the one specimen container. Sometimes a malignant mass may be present amongst other benign masses, and there may be difficulty in identifying the malignant mass’s biopsy location.

Biopsy results should correlate with the appearance and clinical behaviour of the mass. Incisional biopsies are often performed on larger gingival masses, especially when the mass has grown quickly or has become ulcerated. The incisional biopsy sample should be a true representation of the mass incised. This is sometimes difficult especially if the mass has ulcerated or is infected. Inadequate biopsy technique can lead to an incorrect histopathologic diagnosis and this may lead to inappropriate treatment.

The biopsy site should be located in such a position as to be easily included in a possible resection. The treatment plan should include examination/palpation of regional lymph nodes and possible fine needle aspirate of node, oral +/- thoracic radiographs, and consider the aesthetic/functional concerns of the owner if radical local surgery is planned. For most lesions, waiting for incisional biopsy results to accurately plan treatment is encouraged.

In summary

Gingival hyperplasia and the epulides are very common oral growths. Other Odontogenic tumours are less common, but one should always biopsy a suspicious gingival growth, so that appropriate treatment can be instigated.

Further reading

Gardner DG, Epulides in the dog: A review. J Oral Pathol. Med 1996; 25(1):32-37.

Gardner DG, Odontogenic tumours in animals, with emphasis on dogs and cats. 11th. European Veterinary Dental Congress, Granada, Spain. Oct. 2002.

Dubielzig RR, Goldsmith MH, Brody RS. The nomenclature of periodontal epulides in dogs. Vet Pathol 1979; 16:209

Linnick S. Treatment of 2 cases of Acanthomatous Epulis by surgical debulking followed by aggressive ablation using a CO2 laser. 15th Veterinary Dental Forum, San Antonio. Oct. 2001 pgs 112-113

Oakes MG et al., Canine oral neoplasia. The Small Animal Compendium, Jan. 1993 Vol. 15, No.1:15-30.

Reichart PA et al., Epulides in dogs. J Oral Pathol. Med 1989; 18:92-96

Reiter AM, Hypercalcemia in dogs with acanthomatous epulis: A case report and a retrospective study on 59 cases. 11th. European Veterinary Dental Congress, Granada, Spain. Oct. 2002.

Sapp et al., Contemporary oral and maxillofacial pathology. Chapter 5, Mosby

Verstraete F, Odontogenic tumours. 26th. WSAVA congress. Vancouver, Canada. August, 2001.

Yoshida et al., The effect of intralesional bleomycin on canine acanthomatous epulis. J Am Anim Hosp Assoc 1998; 34: 457-461.

Animal Welfare & Poor Dentistry

Dr Wayne Fitzgerald

BVSc (Hons), MANZCVS (Vet. Dentistry & Oral Surgery) Melbourne Veterinary Dentistry

0419-77-4949 wayne_fitz@bigpond.com

Introduction

Animal Welfare Act, 2006, we recognise 5 freedoms of an animal’s needs:

1. Freedom from Hunger and thirst (water and diet) 2. Freedom from discomfort (suitable shelter and bedding) 3. Freedom to express normal behaviour (space, company) 4. Freedom from fear and distress (avoid mental suffering) 5. Freedom from pain, injury and disease (by prevention and rapid diagnosis)

In practice, animal welfare is not always black and white. It often involves ethical and moral issues but we try to make the best decision for the welfare of the animal.

Importantly, we need to realise there is a difference between benign neglect (common) and conscious abuse/cruelty (less common). Both result in animal abuse, but should be handled differently.

Mandatory reporting, the Australian Veterinary Association’s position:

The AVA recommends that veterinarians report suspected animal abuse to the relevant authorities.

The first veterinary priority should be the welfare of the animal. The duty of care should also extend beyond the immediate issue and include prevention of further abuse.

Background

Veterinary dentistry is ‘an ancient art’ practiced on animals of fluctuating importance to man and his civilized evolution. In early times the horse was of more value than the man and as such its care and health was of the utmost importance. This was reflected in the penalties imposed on the ‘practitioner’ who erred in its benefit to the patient.

Many scientific advances are accompanied by changes in socio-economics of a society, this being true of equine dentistry. Prior to the 1800’s horses were heavily used as the primary mode of transportation and draft and their dental needs were high priorities in veterinary medicine. As a testament to the importance of equine dentistry many of the instruments

used today in what we consider ‘advanced’ dentistry were designed or copied from instruments used hundreds of years ago!

At the turn of the 20th century, motorized vehicles began replacing horses as modes of transportation as well as draft use both in urban ‘taxis’ and on farms where tractors began to be used. At the same time, the Great Depression hit and people needed work and families needed to be fed. As a result, the dental needs of horses took a back seat to the greater need to feed people. The veterinary profession focused on problems that more directly affected food production: infectious diseases such as hog cholera, blackleg, anthrax and brucellosis.

In the 1950’s economic growth occurred raising the standard of living of the general population such that families had some disposable income and recreational use of the horse expanded. Additionally, many people began to make their living as trainers for these new professional athletes and an emerging horse industry flourished. The medical needs of horses expanded and many veterinarians developed businesses limited only to the equine patient. As a result, the American Association of Equine Practitioners was founded in the 1954 and continues today as the largest organization of its kind. Still, the dental needs of horses took a back seat to other problems deemed more important, such as colic, lameness and reproduction needs.

As a consequence a door opened: in the 60s many horse owners recognized the need for dental care.

Veterinarians were occupied with other disciplines, this period of waned interest left a vacuum that was filled by laypersons who ‘filed’ teeth and ‘knocked out’ wolf teeth etc. This didn’t unduly concern the profession as the benefit/detriment to the patient was not readily recognized, in any well-publicized scientific manner, and the veterinary profession was unconcerned due to other professional commitments.

In the 1970’s Dr. Gordon Baker, a veterinarian, completed hallmark work advancing the standing of equine dentistry in the veterinary community. Since then, and continuing through to the present day, many advances have been made. Names such as Dixon, Dacre, Kilic, Emily, Easley, du Toit and others continue today to advance equine dentistry within the veterinary profession.

Today, the profession recognizes the importance of a functional and healthy oral cavity to any animal’s health; advances in drugs, technology and skills have allowed this area of science to leap forward far beyond just superficially and blindly ‘floating’ teeth to a position where only qualified and skilled veterinarians can assist.

The AVA recognizes the niche that ‘lay equine dentists’ have carved however, it also recognizes the variables in their levels of training and practise as well as the limitations placed on them by acts such as the Cruelty to Animals Act and the Drugs and Poisons Act which rightly limit their actions within the industry.

In 2008, the AVA Policy Council accepted the Policy on Equine Dentistry and this was followed by Guidelines on dog and cat and then rabbit and guinea pig dentistry.

The aim was to set clear minimum standards and acceptable guidelines for these procedures that could be used to guide practitioners and regulatory bodies. They are also available to the public for reference.

Reports of equine mouth examinations date back centuries but in Germany in the 1930’s, Erwin Becker made significant progressive steps forward in that 80-90 years ago he was regularly performing advanced oral examinations on horses. His instrumentation was impressive and included the use of stocks, full mouth speculum, intra-oral lighting, water irrigation systems, air-driven motorized filing and cutting tools, intra-oral camera and radiology. He even applied many human techniques, such as dental impressions, to the equine patient. His ground-breaking work is still envied today. Unfortunately he was operating in a period where motorcars and machinery were rapidly replacing horses; on top of this it was immediately pre-WW2 where his efforts were not celebrated and passed on nearly as much as they deserved.

This extremely high standard of equine dentistry was well documented in the ‘Becker Tapes’ of which the late Robert Wiggs, past-President of the American Veterinary Dental College, managed to obtain, restore and thus save for future generations.

Note: Some content of the above is courtesy of Dave Klugh, DVM, FAVD / Equine and Oliver Liyou, BVSc (Hons1), MANZCVS

Some horse owners still accept very poor examination and diagnostic techniques by their ‘service provider’. Reasons for this are many, and can include:

The horse’s ability to disguise oral disease Lack of accurate education / awareness and thus owners are not aware that they

may be suffering from oral disease Economic constraints Propaganda by some service providers. Whereby they falsely assure the owner that

the mouth is in good health but leave it in poor health and discomfort after ‘servicing’ the mouth. Statements that support this are “horse’s teeth don’t have nerves” and “horses don’t get periodontal disease”. Reasons for this false reporting may include ignorance and inability to recognize the disease, or fear that they cannot effectively treat the disease and reluctance to refer the case onto someone who can. Having to refer a case may expose the fact that they are not in fact a real ‘dentist’ as they advertise.

In the last few decades we have seen medicine, health and animal welfare awareness rapidly rising again and dentistry has been part of this resurgence. Improved dental exam techniques have resulted in earlier detection and effective treatment of oral diseases in animals, both domestic and exotic.

Background to the AVA Equine Dental Policy:

Equine veterinarians provide dental services to horses around Australia, and are regulated by veterinary legislation in every state and territory.

For many years people without veterinary qualification have been providing equine dental services by rasping and floating teeth, performing teeth extractions and other dental procedures. These dental service providers have not been regulated or accredited with any registration body.

The scientific understanding of equine oral health has expanded considerably in the last few decades and there is now an increased understanding of the animal welfare implications associated with dentistry, in fact there is a much greater understanding of the broader health implications of poor oral health in all animals. For example, problems of the teeth and mouth in the horse can cause weight loss, higher incidence of colic, endocarditis, poor performance and unusual behaviour.

The causes of oral problems in horses are much broader than normal wear and tear of teeth caused by diet or bits. Periodontal disease, abscesses, sinusitis, parasites, tumours, fractured teeth or bones, and congenital problems are just some of the causes of oral problems in horses.

‘Lay’ dental training in Australia:

In 2008, AgriFood Australia developed competencies for a National Certificate IV in Equine Dentistry. This process began some time before and without any input from the Veterinary profession! The AVA was instrumental in obtaining veterinary input* in order to control the documents that were already on the table: Certificate IV and Diploma.

Our professional veterinary input was able to moderate these already developed competencies but it was made clear to us that it was not able to dictate terms or terminate the process.

Eventually a list of competencies for the Certificate IV were accepted (December 2012) and the Diploma was suspended mainly on animal welfare grounds, thankfully supported by a majority of the country’s regulatory bodies.

The only TAFE teaching the Cert IV in Equine Dentistry in Australia at the moment is the Goulburn Ovens Institute of TAFE and all enquiries, student selection and assessment is through and/or by the Equine Dental Association of Australia (EDAA). The job role that this qualification describes includes the title: ‘Certified Equine Dental Service Provider’; the title ‘Equine Dentist’ was to be reserved for the veterinary profession.

* Three members were allowed to join the AgriFood National Reference Group, Drs Bruce Twentyman, Gary Wilson and Wayne Fitzgerald. Dr. David Clarke joined the NRG later on, representing the ANZCVS.

The Certificate IV focuses on the development of the required skills and knowledge to be able to recognize and provide routine dental correction and oral care using manual instruments and complies with all current State/Territory legislation and regulations. It allows for the removal of ‘loose caps’ but not extractions.

In broad terms, there are many non-qualified lay-dentists, some with certificates from non-recognized institutions, here and overseas, working in this country. Some perform advanced oral procedures including extractions and pulp capping and use power tools. The use of ‘sedatives’ by these people is outside of the laws in all States and are often supplied by rogue veterinarians or even veterinary nurses.

A post-operative handout, used by at least one lay dentist, clearly describes what to do when the patient is in severe post-treatment pain. This document demonstrates a number of things: that the treatments may be so severe that demonstrable pain is a factor that should be addressed, that there no real appreciation of how to address that pain, that there is no intention of referring the animal to a veterinarian who may be able to properly address the problem/s. In 2011, at a Victorian Department of Primary Industry round-table discussion concerning equine dentistry, this person described how he used power tools and that when (not ‘if’) he opened a pulp, he applied a dab of Araldite (his version of pulp capping). He vigorously defended this procedure clearly demonstrating the limits of his understanding of the science or the animal’s welfare.

Frustratingly, my presence at this table was of little consequence due to the large and vocal number of lay dentists and non-sympathetic owners present.

I still believe that the statement I made to AgriFood’s NRG is realistic in that “they don’t know what they don’t know!” Science runs a poor second to ‘tradition’.

Professional dental teaching:

There are 7 veterinary schools in Australia, all teach small animal dentistry to some degree but only 2* teach any respectable form of equine dentistry. Of concern it the competition within any tertiary institution’s curriculum for teaching space. Long established disciplines (surgery, medicine etc) fight hard for their long established teaching hours and the newer disciplines, such as dentistry, find it hard to gain ground in this respect. The fact that few vets will ever perform a stifle TPLO in their lives but dentistry and oral surgery will be encountered multiple times daily doesn’t carry much weight …yet.

* Queensland and Western Australia.

The AVDS and ANZCVS provide postgraduate small animal and equine dental instruction in the form of lectures and wet-labs, often in association with the AVA’s annual meeting and Science Week. The AVDS has provided some undergraduate instruction in SA dentistry too. On top of this, there is a significant amount of private assistance and instruction offered to vets in this country.

Dr. Shannon Lee has established and maintains an excellent web site on equine dentistry (equinedentalvets.com.au) and this should be visited if you haven’t yet done so.

There is also ample opportunity for vets and nurses to participate in overseas Continuing Education such as that offered by the American Dental Forum and the European Congress of Veterinary Dentistry.

There are now over 300 vets in Australia that have completed post-graduate CE in equine dentistry and actively practise it; it is not possible to know how many small animal vets have done likewise but interest is keen. The number of lay equine dentists actively working in the field would be less than a tenth of this number but some are aggressively anti-vet and believe in the ‘squeaky wheel’ principal by making a lot of noise. The profession continues to behave professionally and ethically and in this way is getting its message through via ‘best practise’ principles.

Dental treatments:

The AVA and AVDS have Policies, Position Statements and Guidelines on dentistry in common species: dogs and cats, rabbits and guinea pigs and equids. There are clear worldwide positions on ‘sedation’ in the horse for dental procedures as there are for general anaesthesia and analgesia in small animals. The position is that it is not possible to perform a complete, thorough and professional dental/oral treatment without these tools in place.

It is a privilege given to registered veterinarians that they can obtain and use scheduled drugs; the use of such drugs by non-registered persons is clearly illegal for good reasons, the supply of them to lay-persons by veterinarians is unprofessional and does not abrogate the fact that they are responsible for all outcomes. The actions of the profession are firmly controlled by the State Boards and their professional body, the AVA. In contrast, of great concern is the lack of interest or positive action by the responsible bodies: Veterinary Boards (guided by their Acts), the animal welfare bodies (e.g. RSPCA) and the other relevant government departments. It remains that any action by an owner towards a layperson’s inept service or adverse outcomes is generally a civil matter.

As part of the acceptance of the national equine dental Certificate IV competencies, it was put to and accepted by AgriFood that a register and controlling Board be established for these practitioners. To date there has been no action in this regard.

Procedures to be discouraged as contra to good animal welfare:

There are some body tissues that when interfered with can register severe pain: bone and nerves being good examples. Dental procedures generally involve one or both of these structures and the profession is acutely aware of the value of effective analgesia. The benefits are clearly seen in the outcomes even in the face of advanced invasive oral procedures. Our patients tell us how they feel; we just have to be able to read the signs. Ignorance is no excuse in this regard.

Equine unacceptable treatments:

‘Incisor reduction’, often a component of the traditional ‘equilibration’ process, involves the use of cut-off wheels. It was accepted by AgriFood’s NRG that it was considered safe to remove up to 1mm of dentine from the incisors and up to 3mm from cheek teeth, before approaching the sensitive pulps. This practise involves the cutting off of significantly more incisor tooth material than 1mm, the consequences of which can be disastrous for the animal.

The use of power tools without the use of sedation and without the appropriate training in their use. These instruments have the ability to rapidly remove tooth material in an uncontrolled way. The mantra: ‘less is more’ is relevant here and it is possible to not just open pulps but to cause heat necrosis; it is also possible to significantly lacerate soft tissues.

Extraction of wolf teeth. Any dental extraction is an invasive surgical procedure and the common use of a hollow steel punch, for instance, is fraught with adverse consequences. Extractions were clearly disallowed in the Certificate IV competencies developed by AgriFood.

Small animal unacceptable procedures:

Conscious ‘dental prophys’. These procedures are currently actively being promoted by some lay people but have been traditionally performed by pet groomers. At best, the result consists of removing some supragingival calculus with the owner remaining unaware of hidden periodontal issues not detected or addressed, if present, these will continue to progress to the detriment of the animal.

Fractured teeth: there are still vets that consider complicated (pulp exposure) or even uncomplicated crown fractures not to be significant to the animal. The pet may not exhibit obvious pain behaviour but these are painful! Their survival instincts simply override the pain …for the moment at least. Consequences inevitably will be pulp death, infection and ‘abscess’ formation. Clearly the animal’s welfare is compromised.

Reshaping or crown modification practises often lead to pulp exposure and/or pulp death. The cat’s mandibular canine teeth are a good example as extraction of the maxillary canine tooth often leads to penetration or trauma to the upper lip, as the pulp of the lower canine is very close to its crown there is no room to simply crown-reduce the sharp tip in an effort to solve this issue.

Malocclusion. Many are ‘traumatic’ meaning they cause significant immediate or delayed physical issues for the animal but the behavioural issues (such as guarding or head-shyness in a dog) are often not properly recognized.

Of significance in rabbits is the development of ‘slobbers’, weepy eyes and facial abscesses secondary to occlusal problems. Ignoring malocclusions is inappropriate and professional advice should be sought. The advertisement example below promotes dog and cat teeth cleaning without sedation or anaesthesia by Brian Borg. He has also appeared on television promoting this service.