Periodontology

Introduction

Periodontal disease is not a new disease. It has affected both man and animal kind since they first appeared on the earth. Periodontal diseases have been reported as one of the most common diseases of the Egyptians more than 4,000 years ago. In one of the oldest Chinese medical books from 2,500 B.C., there is a chapter devoted to dental and gingival diseases. The importance of oral hygiene was also recognised by ancient civilizations, including the early Hebrews and Phoenicians, who had used wire splinting to stabilise teeth loosened by chronic periodontal disease.

Early works and case reports have been published in veterinary literature. Colyer published a complete book on the ‘Variations and Disease of Teeth of Animals’ in 1936. A case report was published in the Journal of Comp. describing false teeth for a dog in 1897. GV Black also reported on ‘pyorrhea’ in dogs at the end of the 1800s, confirming dogs from this era suffered from periodontitis and periodontal disease. But most of the advancements in small animal dentistry, especially periodontal disease, have been since the 1970s. The biggest leaps forward have been: 1. The setting up of dental societies around the world: 2. Establishment of a specialist veterinary dental college in the US and Europe: 3. Commercial companies developing instruments and materials for the treatment of established periodontal disease: and 4. Pet food companies manufacturing diets for the reduction of plaque and calculus.

Anatomy

The periodontal tissues, also termed the periodontium, consist of: the alveolar bone, gingiva, cementum and periodontal ligament.

Periodontal tissues – Upjohn Animal Health poster.

The maxilla and mandible contains the alveolar processes, which is effectively the bone surrounding the tooth sockets. The processes consist of the alveolar bone (or cribriform plate), compact bone and cancellous trabeculae bone. The alveolar bone lines the tooth sockets, radiographically appearing as a thin white, radio-opaque line, termed the lamina dura. In health, the lamina dura parallels the periodontal ligament. The compact bone covers the outer surface of the processes. The trabecular bone lies between the processes.

The healthy tooth is composed of two major parts: the supra-gingival portion that extends above the gingiva and is grossly visible, termed the crown, and the sub-gingival portion that extends beneath the gingiva, termed the root. A central cavity is located within the tooth, termed the pulp canal (located in the root segment) and pulp chamber (located in the crown segment). The pulp, which consists of nerves, blood vessels and connective tissues, is located within the pulp canal and chamber. It provides nutrition and sensation to the tooth. The pulp is surrounded and therefore protected by two hard layers. An inner layer composed of dentine, which is found in both the crown and root, and an outer layer of enamel and cementum. The crown is covered in enamel. The root has an outer covering of cementum. The point where the crown and root meet is termed the cemento-enamel junction. In 30% of teeth, the enamel meets the cementum with no overlap, i.e. an edge-to edge join, in 65% of teeth the cementum overlaps the enamel, and in 5% of teeth there is a gap, which means dentin is exposed to the gingival sulcus. This means that odontoblasts are exposed to the gingival sulcus or periodontal pocket.

Diagram of the tooth.

The periodontal ligament is a connective tissue that supports and holds the tooth in the alveolus. It also supports and cushions the tooth from external forces. The ligament is composed of collagen and elastic fibres arranged in bundles or groups, with one end attaching to the cementum on the tooth root and the other end attaching to the maxillary / mandibular alveolar bone (cribriform plate). At the point the fibres embed into the cribriform plate, they are termed Sharpey’s fibres. The periodontal ligament contains blood vessels, lymphatics and nerves. Fibroblasts are the most common cell-type in the periodontal ligament. Their role is two-fold: 1. Produce collagen, 2. Possess the capacity to phagocytose old collagen fibres and degrade them by enzyme hydrolysis. Thus, collagen turnover is regulated by the same cell type. The blood supply is derived from the superior alveolar artery for the maxilla and the inferior alveolar artery for the mandible, venous drainage accompanies the arteries. Nerve supply is via branches of the trigeminal nerve. The ligament relies on occlusal forces to keep it functional, if forces are diminished or absent, the ligament atropies and the teeth eventually become mobile and are exfoliated.

The gingiva, a stratified squarmous epithelium, is the part of the oral mucosa that covers the alveolar processes and surrounds the teeth. In the majority of animals, after the tooth has erupted to full crown height, the gingiva attaches permanently to the tooth at the cemento-enamel junction. This attachment is via a junctional epithelium and is termed the epithelial attachment. The epithelial attachment consists of a collar-like band of stratified squarmous non-keratinising epithelium. The gingiva can be divided into two regions: the free gingiva (which lies coronal to the epithelial attachment, is mobile, and does not attach to the tooth surface) and the attached gingiva (which lies apical to the epithelial attachment, is not mobile and attaches to the periosteum of the underlying bone). The space created between the free gingiva and the tooth surface is termed the gingival sulcus. In healthy pathogen-free animals, the gingival sulcus is V-shaped and barely allows penetration with a periodontal probe. Once a bacterial population is established within the oral cavity, the sulcus enlarges and the probing depth is normally 0 – 0.5mm in cats and 2 – 3 mm in dogs.

Diagram of tooth and gingival sulcus – Virbac poster on periodontal disease.

What’s normal?

Healthy oral cavities have a number of characteristics. The attached and free gingiva should be coral pink in colour but may vary due to the vascular supply, the thickness of the epithelium and the presence of pigments. The attached gingiva should be firm and stippled. Stippling, which appears as a texture similar in appearance to an orange peel skin, is a form of reinforcement against disease and dietary abrasion. Once the tissue suffers gingivitis, the stippling disappears, but returns when health is restored. The teeth should be white, exceptionally white as compared to the discoloured teeth of people who drink coffee and smoke. This means, accumulations of plaque and deposits of calculus should not be present. Even the little specks of calculus that we see during the annual health check and vaccination and all think are normal, should not be present. Thus don’t tell the client ‘there’s only a little bit of calculus on the teeth, let’s see how it is next year’. Treatment should be performed immediately, including scaling and polishing and a homecare program instituted.

Healthy tooth and gingiva.

Causative Factors

Periodontal disease is the most common infectious disease in the world, affecting over 85% of all dogs and cats over 2 years of age. It is a multi-factorial disease that requires the presence of a number of factors simultaneously. In the past, many veterinarians have considered periodontal disease to be in the same basket as any other infection, but it is not the same, as it is the only infection that occurs on a hard tissue that erupts through a soft tissue. Some of the factors that influence the progression of periodontal disease include distribution of plaque, virulence of the individual microflora, calculus deposits, the dog or cat breed, type of bite, malocclusions, tooth rotation or overcrowding, genetics and immune factors, general health, age, home dental care, chewing behaviour, saliva, muzzle hair, periodontal pocket depth, inflammatory status just to mention a few. Therefore, we need to treat both the infection, as well as deal with the other factors. Otherwise we will fail to control the infection, and we will not be able to maintain the health of the periodontal tissues.

Although periodontal disease is a multi-factorial disease, the primary cause is plaque. In a healthy dog or cat eating a meaty ‘natural’ diet, the meat must be chewed prior to swallowing. The action of the teeth penetrating and tearing the meat and tissues abrades the majority of the plaque from the tooth surfaces. Therefore, if the tooth surface does not undergo mechanical abrasion by the diet, plaque accumulates on the tooth crown.

How does plaque form?

Supra-gingival tooth surfaces are constantly bathed in saliva. Throughout the day and night, an invisible acellular layer of salivary and alimentary glycoproteins, polypeptides and lipids, termed the ‘pellicle’, attaches to the supra-gingival tooth surface. Following pellicle formation, Gram positive aerobic bacteria attach to the pellicle and proliferate. The mixture of pellicle, bacteria, food and saliva develops into a biofilm, termed ‘plaque’. Plaque takes about a week to form a mature colony. Plaque is not a food residue, as it actually forms more rapidly during sleep and less rapidly when food is consumed. Plaque cannot be seen unless it is stained.

Erythrosine stained plaque appearing as pink to dark red on the supra-gingival tooth surface.

Gingivitis

With supra-gingival plaque formation, and contact with the free gingiva, gingivitis develops. Gingivitis is an inflammation of the gingiva. The dominant bacteria in the early stages of gingivitis are Actinomyces viscosus and Streptococcus sanguis. The clinical signs of gingivitis are oedema, hyperplasia, hyperaemia, haemorrhage, inflammation, oral pain, and halitosis. Inflammation is characterised with changes such as vasodilation of capillaries, adherence of neutrophils to vessel walls, leukocytes leaving the capillaries through vessel walls, followed by an increase in collagen destruction, and neutrophils engulfing and phagocytosing bacteria. If the inflammation continues, neutropenia may occur, as well as an increase in plasma cells and macrophages, production of lysosomes and acid hydrolases, and eventually permeability of the epithelial attachment and movement of the bacteria and inflammatory process into the deeper structures of the periodontal tissues.

Gingivitis adjacent to the maxillary right fourth premolar (108) in a cat.

Unless the plaque is removed, it extends sub-gingivally. In the early stages of the disease, there is little difference in the bacteria populations and compositions between supra- and sub-gingival plaque, of which aerobes comprise 75% and anaerobes 25% of the population.

Diagram of tooth and sub-gingival plaque – Virbac poster on periodontal disease.

Subgingival changes

Once plaque extends sub-gingivally, changes occur. Aerobic bacteria consume the oxygen, reducing the redox potential, thus creating a more suitable environment for anaerobic bacteria to establish themselves. Inflammation extends further sub-gingivally, with subsequent oedema and hyperaemia of the free gingiva, resulting in a deepening of the periodontal sulcus, termed a pseudo periodontal pocket. With the development of sub-gingival inflammation, the conditions are set for periodontitis to develop.

Periodontitis

Periodontitis is the active inflammatory disease state of the gingiva, alveolar bone and periodontal ligament. Gingivitis always precedes periodontitis. It is common to read the human texts that state ‘but not all gingivitis develop into periodontitis’. This may be true in humans, but as a general rule in veterinary dentistry, the majority of dogs and cats with gingivitis will eventually suffer periodontitis.

As the sub-gingival redox potential continues to decrease, the environment heavily favours the production of anaerobic bacteria. The primarily anaerobic bacteria responsible for destruction of the periodontal tissues are Gram negative: Porphyromonas spp. (previously black-pigmented Bacteroides), Prevotella spp., Peptostreptococcus spp., Fusobacterium spp. and the spirochetes. High levels of Porphyromonas spp. have consistently been associated with progressive periodontitis in the dog. There is a direct relationship between an increase in Porphyromonas gingivalis and a deepening of the periodontal pocket. Interesting though, with a deepening of the periodontal pocket, the gross number of sub-gingival aerobes do not differ from those in the supra-gingival population, whereas the gross number of anaerobes increase significantly. The sub-gingival anaerobes in a healthy gingival sulcus comprise 104 colony forming units (CFU) / cc3. As the periodontitis advances and the periodontal pocket deepens, the number of anaerobes can increase to 108 CFU / cc3. Eventually anaerobes constitute 95% of the sub-gingival population. No sub-gingival site harbors a pure culture of a single bacterial species, it is a true-mixed population, with over 300 different bacterial species cultured from some of the human periodontal pockets. Therefore interactions between species are a critical component in the progression of the disease.

Periodontal pockets

A periodontal pocket is established when the probing depth is greater then 3mm in a dog and 0.5mm in a cat. The beginnings of a periodontal pocket occur when bacteria make contact with the epithelial attachment, the host’s immune system is unable to control or eliminate the endotoxins produced by the bacteria and the immune system produce inflammatory mediators that induce damage to the periodontal tissues. The transformation of the sulcus into a periodontal pocket creates a void where plaque cannot be mechanically removed by diet alone. Continued growth of plaque induces a destruction of and apical migration of the epithelial attachment. This results in the loss of the periodontal ligament and alveolar bone. This now becomes a progressive disease. In reality, periodontitis does not progress in a constant regular fashion, as the advancing disease is halted by the immune system every now and again. Periodontal disease is actually a disease of quiescence with random bursts of activity.

Diagram of formation of a periodontal pocket. Plaque and calculus attachment to the tooth root and loss of attachment including periodontal ligament and alveolar bone – Virbac poster on periodontal disease.

Periodontal pockets are best seen as chronic inflammatory lesions that are constantly undergoing repair. The epithelium lining is continually inflammed and infected. Because the epithelium lining of the periodontal pocket is a semi-permeable membrane, there is a constant stream of bacteria, bacterial by-products and inflammatory mediators entering the gingival tissue, and thus, entry into the systemic circulation. This in turn, may result in a systemic infection and possibly endocarditis, glomerulonephritis and meningitis, which have all been reported in the human literature. In time the cementum will be infiltrated with bacteria, endotoxins, plaque and calculus. Bacteria may penetrate the dentinal tubules, resulting in cementum caries, cementum necrosis, pulpitis and pulp necrosis with internal and external resorption.

Vertical and horizontal bone loss

As periodontitis progresses, the inflammatory process produces resorption of the alveolar bone and loss of the periodontal ligament. This may occur around a single tooth root, and is termed vertical bone loss, or vertical periodontitis. Or it may proceed in a horizontal direction affecting adjacent roots, and exposing the furcation areas, and is termed horizontal bone loss, or horizontal periodontitis. If gingival recession occurs, as is often the case with Poodles, the furcation is exposed. If no gingival recession occurs, the periodontal pocket continues to deepen. This allows more plaque to enter the pocket and further tissue damage occurs. Radiographically, vertical and horizontal bone loss has characteristic features. Vertical bone loss occurs around a single tooth root, ie on the palatal side of the maxillary canine in a Dachshund dog. Horizontal bone loss appears as a reduction in the alveolar bone height over a number of tooth roots.

Pocket depth and loss of attachment is not necessarily the same. Pocket depth is measured and expressed as the distance from the epithelial attachment to the free gingival margin. Attachment loss is measured as the distance from the epithelial attachment to the cemento-enamel junction.

Gingival recession, horizontal bone loss and furcation exposure in the maxillary premolar teeth in a dog.

Radiograph of vertical alveolar bone loss surrounding the root of the maxillary right first premolar tooth (105) in a dog. Note radiolucency of bone.

Radiograph of horizontal alveolar bone loss extending across mandibular left 3rd (307) and 4th (308) premolar teeth in a cat. Note radiolucency of bone, loss of coverage of root and furcation exposure.

Complications of mandibular alveolar bone loss

Eventually the periodontal pocket will reach the apical tip of the tooth and there will be inadequate support to keep the tooth in the mouth. Exfoliation may result. Another common scenario is loss of alveolar bone to the point where moderate trauma results in pathological fracture. This is occurs in small breed dogs and usually is adjacent to the canine tooth or the first molar. Treatment options will be discussed in oral surgery.

Pathological fracture of mandible following a dog fight. Note the existing periodontal disease and horizontal alveolar bone loss from the fourth premolar to the 1st molar teeth.

Pathogenesis

Although the pathogenesis of periodontal disease is not completely understood, it is now well accepted that the host’s response to plaque, rather than its direct actions is responsible for the damage done. Two hypotheses have been described: 1. Neutrophils and macrophages are attracted to the area, produce collagenase and other lysosomal enzymes, which destroy collagen: 2. Fibroblasts phagocytise collagen fibres by extending cytoplasmic processes to the ligament-cementum interface. The coronal portion of the epithelial attachment is subject to increased invasion of neutrophils, which subsequently detaches from the tooth surface. Thus, the bottom of the sulcus shifts apically and the sulcular epithelium occupies a gradually increasing portion of the sulcus lining.

Gram negative bacteria are capable of producing a wide variety of bioactive molecules that affect the host including lipopolysaccarides (LPS), proteases and other cytotoxic molecules. The predominant leukocyte in the blood in the neutrophil. It is also believed to be the initial and predominant defence cell in the periodontium. Porphyromonas gingivalis has been shown to possess an arsenal of proteases, which can cleave immunoglobulins preventing opsonization of the bacteria. Macrophages are a major component in the host response to periodontitis. Macrophages are stimulated by bacterial stimuli, which then secrete interleukin 1B (IL-1B), tumour necrosis factor A (TNF-A) and prostaglandin E2 (PGE-2). IL-1B is a cytokine that is produced primarily by macrophages, which have been stimulated by LPS, which has an action of bone resorption. The main cellular source of TNF-A is tissue macrophages. TNF-A also has the capacity to stimulate bone resorption. Unlike the cytokines, the prostaglandins are short acting lipids from arachidonic acid released from damaged cell membranes by phospholipase A2. LPS is one of the potent stimulators of PGE-2 secretion by macrophages and is a potent mediator of bone resorption. Studies have shown there is more PGE-2 in diseased sites than in healthy tissue and levels are related to periodontal disease progression.

Calculus

Both supra-gingival and sub-gingival plaque is continually bathed in calcium rich saliva, which undergoes mineralization to form calculus. Calculus in the dog is primarily composed of calcium carbonate, whilst in the cat it is a carbonate containing hydroxyapatite. Supra-gingival calculus is brown-grey, soft and easily removed compared to sub-gingival calculus, which is dark brown-black in colour and often difficult to remove. Calculus is heavily deposited adjacent to the salivary duct openings. Calculus itself does not initiate nor promote gingivitis. Calculus tends to promote further plaque accumulation, as it has a very rough surface.

Accumulation of calculus of the supra-gingival buccal tooth surfaces in a dog.

Accumulation of calculus of the supra-gingival buccal tooth surfaces in a cat.

Disease Types

There are two broad sub-groups of juvenile periodontal disease and three sub-groups of adult periodontal disease.

Juvenile diseases include:

• Juvenile gingivitis
• Juvenile onset periodontitis

Adult diseases include:

• Slowly progressing periodontal disease (also termed ‘adult’)
• Rapidly progressive periodontitis
• Refractory periodontitis

Juvenile gingivitis

Juvenile gingivitis is commonly observed prior to or at the time of teething. Dogs have a marginal gingivitis, seen in Shar Pei and some of the toy breeds, that following teething returns back to healthy gingiva. Kittens, especially Abyssinians, Persians and ginger-coated farm cats often suffer feline juvenile gingivitis at the time of teething that appears as a hyperaemic, proliferative gingivitis, with minimal plaque and calculus. The teeth can be totally covered by the hyperplastic gingiva, forming a pseudo pocket. Cultures and biopsies are non-conclusive. Aetiology is unknown.

Severe gingival hyperplasia and hyperaemia in a cat.

Juvenile onset periodontitis

Juvenile onset periodontitis affects kittens before 9 months of age, with most being sickly with an upper respiratory tract infection. I’ve mainly seen this in Siamese and domestic short hairs. Dog breeds affected are the Maltese, Miniature Schnauzer and Greyhounds. Onset is just prior to or at the time of teething, with a huge amount of plaque and rapidly forming calculus on all buccal tooth surfaces with severe ulceration of the muco-gingival tissues. Clinical signs include gingival recession, periodontal pocket formation, furcation exposure and horizontal alveolar bone loss. Aetiology is unknown in the cat, but it is highly likely that respiratory viruses may be involved including Calicivirus and Herpesvirus. In the dog, aetiology is also unknown, but may have spirochete involvement, an auto-immune/immune mediated disease or possibly hyper-reaction to bacterial endotoxins, but this is open to more research.

Slowly progressive adult periodontal disease

This is the most common form of periodontal disease we see in veterinary practice. It is slow to progress, increasing in severity throughout the animals’ life, seen clinically as generalised gingival inflammation in the early stages, followed by accumulations of plaque and calculus and advancing to periodontitis with gingival recession or pocket formation.

Stages of Adult-onset Periodontal Disease
First Stage = Early gingivitis. Minimal plaque and calculus. Mild gingival inflammation, no bleeding on probing, normal gingival sulcus depth.

Second Stage = Advanced Gingivitis / Early periodontitis. Increased plaque and calculus. Gingival oedema, bleeding on probing, loss of attachment or moderate pocket formation with up to 25% loss of alveolar bone height.

Third Stage = Established Periodontitis. Moderate plaque and calculus. Loss of attachment or moderate pocket formation with up to 50% loss of alveolar bone height. There may be slight tooth mobility.

Fourth Stage = Advanced Periodontitis. Large deposits of plaque and calculus. There is advanced pathology of the periodontal tissues with severe pocket depth (greater than 50% attachment loss) or severe recession. The tooth is mobile.

Rapidly progressive periodontitis

This affects young mature animals, generally over 12 months of age. Clinically we see extensive attachment loss, deep periodontal pockets, excessive inflammation and ulcerative mucosal areas, all as a direct result of plaque intolerance and excessive host immune response to the plaque. The breeds commonly affected are the Maltese, Yorkshire Terriers and Greyhound dogs, and Burmese and Oriental breed cats. Most animals have antibodies to Actinobacillus sp. and Porphyromonas gingivalis, as well as developing neutropenia or defects in neutrophil chemotaxis.

Severe gingival recession and localised buccal mucosal ulceration (kissing ulceration) in a dog.

Refractory periodontitis

This can be regarded as an extension of rapidly progressive periodontitis, as it occurs in the breeds mentioned and also Miniature Schnauzer dogs, and cats with established lymphocytic, plasmalytic stomatitis. Clinically the mucosa is ulcerated, especially where the mucosa contacts the buccal surface of the canine and 4th premolar teeth. There is often gingival recession with root and furcation exposure.

Severe gingival hyperplasia, plaque and calculus accumulations and generalised mucosal ulceration in a dog.

The veterinary treatment of periodontal disease involves the mechanical removal of plaque and calculus. I do not believe that you can scale the teeth adequately without the patient under general anaesthesia or using only electrical or air driven equipment. Therefore, to complete the procedure properly, general anaesthesia and hand instruments must be used.

I use the following list as a guide to teeth cleaning, which I also use to explain the process to clients.

Treatment recommendations for Periodontal Disease Types

Juvenile gingivitis

Juvenile gingivitis is commonly observed prior to or at the time of teething. Dogs have a marginal gingivitis that following teething returns back to healthy gingiva. Kittens gingivitis at the time of teething appears as a hyperaemic, proliferative gingivitis, with minimal plaque and calculus. The teeth can be totally covered by the hyperplastic gingiva, forming a pseudo pocket. Cultures and biopsies are non-conclusive. Aetiology is unknown. Treatment requires a gingivectomy with electrocautery or a cold scalpel to remove the pseudo pockets followed by teeth cleaning. Antibiotics and corticosteroids may be palliative. Homecare is often beneficial.

Juvenile onset periodontitis

Juvenile onset periodontitis affects kittens before 9 months of age, with most being sickly with an upper respiratory tract infection. Dog breeds affected just prior to or at the time of teething, with a huge amount of plaque and rapidly forming calculus on all buccal tooth surfaces with severe ulceration of the muco-gingival tissues. Clinical signs include gingival recession, periodontal pocket formation, furcation exposure and horizontal alveolar bone loss. Aetiology is unknown in the cat, but it is highly likely that respiratory viruses may be involved including Calicivirus and Herpesvirus. In the dog, aetiology is also unknown. Treatment involves diligent scaling and polishing, extensive teeth extraction, followed by vigorous homecare, including Oravet, SANOS, Maxiguard and daily toothbrushing. Most of the antibiotics do not have long lasting effects. Usually the pet has to come back at regular intervals for further teeth cleaning and selective extractions. Eventually, the pet may end up with no teeth, because the owners are not able to control the disease process.

Slowly progressive adult periodontal disease

This is the most common form of periodontal disease we see in veterinary practice, seen clinically as generalised gingival inflammation in the early stages, followed by accumulations of plaque and calculus and advancing to periodontitis with gingival recession or pocket formation. Treatment success can be achieved with teeth cleaning (scaling and polishing), local antibiotic delivery systems in deep periodontal pockets and adequate client home care (removal of plaque re-attachment).

Rapidly progressive periodontitis

This affects young mature animals, clinically we see extensive attachment loss, deep periodontal pockets, excessive inflammation and ulcerative mucosal areas, all as a direct result of plaque intolerance and excessive host immune response to the plaque. Treatment success is difficult, as most do not respond to conventional treatment or will reoccur after treatment. Treatment success can be achieved in the short term with teeth cleaning, use of metronidazole 10mg/kg bid and clindamycin 11mg/kg bid, and extensive diligent homecare. Homecare will include Oravet, SANOS, Maxiguard, application of local anaesthetic gels to the mucosa, placement of chlorhexidine soaked swabs to the affected mucosa or chlorhexidine rinses/washes into the mouth, and daily toothbrushing. Long-term success may involve selective extractions and long term use of antibiotics, NSAIDs or prednisolone. Anti-inflammatories can be used in the short-term, but rarely control the pain or inflammation in the long-term.

Refractory periodontitis.

This can be regarded as an extension of rapidly progressive periodontitis. Clinically the mucosa is ulcerated, especially where the mucosa contacts the buccal surface of the canine and 4^th premolar teeth. There is often gingival recession with root and furcation exposure. Long-term treatment success is difficult. Professional meticulous scaling and polishing of the teeth, sometimes as often as every 3 – 6 months, selective extraction of teeth in contact with the mucosa and causing ulceration, debridement of mucosal lesions, extended use of antibiotics including metronidazole 10mg/kg bid, clindamycin 11mg/kg bid, anti-inflammatories including NSAIDs and prednisolone and diligent homecare by the owners. The inflamed areas are often so painful that owners are unable to handle the dog’s mouth. Also, following extraction, the inflammation often occurs in a new location.

Dental Treatment Protocol

1. Pre anaesthetic check and gross oral examination
2. Pre anaesthetic pathology (blood work and urine analysis)
3. Administration of antibiotics and/or anti-inflammatories/analgesics
4. Administration of intravenous fluids
5. General anaesthesia
6. Operator protection (Mask, Gloves, Face Shield)
7. Gross oral examination (record findings on dental chart – www.vetdentalcharts.com)
8. Periodontal Probing (record findings on dental chart – www.vetdentalcharts.com)
9. Gross removal of supra-gingival plaque and calculus
10. Radiology
11. Sub-gingival scaling (root planing and sub-gingival curettage)
12. Polishing
13. Sulcular Irrigation
14. Extractions (if necessary)
15. Guided tissue rejuvenation – local delivery antibiotics (Doxirobe / pluronic gel)
16. Guided tissue regeneration (Consil / membranes)
17. Placement of barrier sealants (Oravet / SANOS)
18. Discharge animal with home care instructions

Why perform periodontal scaling?

The rationale for treatment is:

1. Removes plaque and calculus from the tooth surface
2. Removes diseased cementum and endotoxins on root surface
3. Decreases the quantity of bacteria present on the tooth surface and in the periodontal pocket
4. Provides a smooth tooth and root surface that decreases rate of plaque re-attachment
5. Provides a clean root surface for pocket epithelium reattachment
6. Provides a clean tooth surface which the owner can keep clean
7. Relieves pain and inflammation
8. Allows placement of local delivery antibiotics

Thus, the primary purpose of general anesthesia and teeth scaling is to reduce the quantity of pathogens to a level that decreases inflammation and provides an environment for the host’s immune system to commence healing. Regeneration and repair are the aim. In an ideal world, the periodontal tissues would regenerate and new alveolar bone and periodontal ligament would grow and a normal gingival sulcus would form. In reality, in the majority of cases, this does not occur, and what we achieve is repair with a fibrous attachment of the pocket epithelium to the root cementum. A gingival sulcus forms but is not as resistant to plaque re-attachment, inflammation and destruction as before. But still, a healthy inflammation free area can be achieved.

When is scaling needed:

I would clean the teeth when any one of the following is present:

1. Gingivitis
2. Erythrosine stains plaque on the majority of teeth
3. Calculus is present on any tooth
4. Animal has halitosis
5. Gums bleed on probing
6. There are ulcers on the gingival or mucosal tissues
7. Furcation exposure
8. Tooth mobility
9. Pus is elicited from the sulcus or pocket on gentle palpation

Antibiotics

As the majority of periodontal disease is caused by anaerobic bacteria and spirochetes, the most effective antibiotics for dental use are amoxicillin, amoxicillin/clavulanic acid, clindamycin, doxycycline and metronidazole. Are antibiotics needed in the majority of dental disease, probably not. See article on ‘Prudent Use of Antibiotic Usage in Dentistry’ in the article downloads.

When needed amoxycillin and amoxycillin/clavulanic acid combination is prescribed at 10mg/kg bid. Clindamycin is prescribed at 5.5mg/kg bid for gingivitis and 11mg/kg bid for osteomyelitis. Clindamycin is able to penetrate the biofilm layer of plaque. Doxycycline is prescribed at 2.5 mg/kg sid-bid. Doxycycline has two primary actions: anti-bacterial and anti-collagenase. At the low end of the dose, doxycycline is bacteriostatic, whereas at the high end of the dose it is bacteriocidal. Doxycycline binds to 2+ cations such as calcium, as well as being concentrated and secreted in the crevicular fluid at four times the blood plasma levels. Doxycycline can be used as a local delivery antibiotic, as it is available in a gel form, called Doxirobe, which can be injected into periodontal pockets after root planning. Metronidazole is an antibiotic that possesses both anti-bacterial and anti-inflammatory properties when prescribed at 10mg/kg bid, has 100% susceptibility against anaerobic bacteria, therefore is ideal for use in anaerobic periodontal disease involving Porphyromonas gingivalis.

Studies have shown that antibiotics prescribed 48 hours prior to the dental procedure will reduce the bacteremia and bacterial aerosol produced during sub-gingival and supra-gingival scaling respectively.

Analgesia

The tooth root is composed of thousands of dentinal tubules, all containing an odontoblast, which transmit pain when stimulated. Therefore root planning is a painful procedure. Pre-anaesthetic analgesia can be achieved with opioids and NSAIDs. Anaesthetic agents such as ketamine also have analgesic properties. Local anaesthetics and regional nerve blocks should also be considered as an adjunct to the standard analgesics.

Intravenous fluids

The placement of intravenous fluids should be commenced prior to pre-medication. As per normal physiological effects of anaesthetic agents, ie hypotension, fluids aid in maintaining blood pressure and glomerular blood flow, thereby decreasing potential renal complications. This is especially important in older cats. There have been many anecdotal reports and journal articles discussing the case where an old 18 year-old cat comes into the surgery for a ‘dental’, no fluids are given, and the cat suffered renal failure two weeks after the procedure.

General Anaesthesia

All animals should have a general anaesthetic for dental procedures. A cuffed endotracheal tube should be used to prevent water and aerosols, produced during scaling, entering the trachea and lungs. The pharynx should be packed with bandage, swabs or a tampon to prevent calculus falling into the pharynx. Remember to remove them after the procedure. If swabs are used and tied together with bandage or string, I then either tie the free end to the endotracheal tube or leave it hanging out of the animal’s mouth.

General anaesthesia and endotracheal tube placement in a cat.

Monitoring

Anaesthesia monitor should be performed by an assistant and mintoris and recorded every 5 minutes.

Self protection

You should wear glasses to protect the eyes from flying calculus and a mask to prevent inhalation of the bacterial laden aerosols. There have been anecdotal reports of veterinarians suffering from corneal abrasions, one veterinarian in Canada losing an eye, another in New Zealand with severe keratitis and calculus imbedded his the cornea, and numerous students after veterinary dental practicals with sore eyes and respiratory disease, coughing etc. Therefore, it would be prudent to wear a mask and safety goggles or glasses whilst performing dental procedures.

‘Gretel’, modeling as my trusty assistant, demonstrates wearing a mask and eye protection.

Equipment

Every good sportsman needs good equipment, the cricket bat, the tennis racquet, racehorse etc. The veterinary dentist needs the PROPHY KIT, which should contain:

1. Periodontal probe
2. Explorer
3. Dental Mirror
4. Supra-gingival scalers
5. Sub-gingival curettes
6. Tartar removing forceps
7. Minnesota retractor
8. Barrier sealant (Oravet/SANOS)
9. Rejuvenation products (Doxirobe/plurnic gel)
10. Regeneration products (Synergy/membranes)

Probing and Charting

Periodontal probes are used to determine the position of the epithelial attachment and thereby measure the depth of the gingival sulcus and periodontal pockets.

To determine the depth of the gingival sulcus or periodontal pocket, the graduated periodontal probe is placed along the root surface, under the gingival margin, until it reaches the resistance of the epithelial attachment. Gentle force should be used, as it is easy to penetrate through inflammed tissues. The depth of the sulcus or pocket is measured in millimetres from the gingival margin to the epithelial attachment. Measurements are made in two to three places on the buccal surface and two to three places on the lingual/palatal surface of each tooth. If the gingiva has receded, then the measurement from the epithelial attachment to the cemento-enamel junction gives the loss of attachment. The depth of the pocket, as well as, gingival recession should be recorded on the dental chart. Healthy periodontal tissues exhibit pocket measurements of 0 – 0.5mm and 2 – 3 mm in the cat and dog respectively. Therefore, measurements of 1mm or greater in cats and 4mm in dogs indicate attachment loss.

Diagram of ‘how to use a periodontal probe’.

Placement of the periodontal probe to measure periodontal pocket depth of 10mm of the mandibular 3^rd incisor tooth.

Periodontal probes are typically a metal or plastic tapered rod with a blunt end attached to a handle graduated in millimetre markings. There are several types available. The Williams, Marquis, Michigan-O and Nabors, are the most common types. Selection is by personal preference. The most common is the Williams, which is graduated in millimeters at 1, 2, 3, 5, 7, 8, 9 and 10 mm. I like the Williams probe, as I find that the markings are easy to read. The Marquis has alternating dark and light bands in 3mm segments at 3, 6, 9 and 12 mm. On the Marquis probe, I have found the markings fade with continued autoclaving.

The ‘Williams’ periodontal probe.

The Michigan – O is graduated at 3, 5 and 8mm. The Nabors, which has no markings, is curved and ideal for examination of a furcation defect. It could be argued it is more of an explorer than a probe. Often in veterinary dentistry, an explorer probe is attached to the opposite end of the periodontal probe. It has a sharp needle point that can be utilized to examine furcation defects, sub-gingival calculus deposits, resorptive defects and cavities, just to name a few.

Dental Charts

All pathology, including the periodontal sulcus and pocket depths, plaque, gingivitis and calculus may also be recorded on the chart. These can be designated using a numbered index which represents the degree of plaque, gingivitis of the gum and the amount of calculus on the tooth surface. An example of a canine and feline dental chart is available at www.vetdentalcharts.com. The pathology is represented by symbols or letters used by the American Veterinary Dental College, www.AVDC.org.

Gingivitis Score

The gingivitis score gives the practitioner a score that is directly related to the degree of gingivitis present based on the following:

0 = no gingivitis present

1 = mild gingivitis, inflammation of the gum, no bleeding on probing

2 = moderate gingivitis, delayed bleeding on probing

3 = advanced gingivitis, immediate bleeding on probing

Plaque Scoring

Plaque can be disclosed using a dye. One stage dyes stain all plaque the same color. Two stage dyes stain new and old plaque different colours. Fluorescein dyes require an ultraviolet light to visualize the plaque. The greater the thickness of plaque on the tooth surface, the darker the dye. The most common one stage dye is erythrosine. Prior to cleaning the teeth, a drop of 2% erythrosine is placed on the supra-gingival tooth surface and washed off with a gentle stream of water, from the triplex on your dental machine or via a 10cc syringe and 22 gauge needle.

Erythrosine can also be used to demonstrate plaque accumulation to clients. When the client brings the pet into the consulting room, place a drop of erythrosine onto the canine and maxillary 4^th pre-molar teeth. Wait five minutes. The plaque will be stained pink and provides an ideal visual demonstration to the client that their pet’s teeth require cleaning. Erythrosine can also be used prior to cleaning and post-cleaning as a way to confirm you or your staff, are adequately cleaning the teeth. It can also be used at client revisits, to confirm homecare is adequate.

In the clinic, a simple plaque scoring system can be used as follows, based on coverage:

0 = No observable plaque

1 = Less than 25% coverage

2 = Between 25% and 50% coverage

3 = Between 50% and 75% coverage

4 = Between 75% and 100% coverage

Erythrosine staining of plaque on the buccal surface of the teeth in a dog.

Plaque scoring is also useful to compare diets that claim plaque reducing effects, such as Royal Canin Dental diet, Hills t/d diet and Eukanuba DDS. The scoring that is performed produces a number, called the Plaque Index. Many authors have put their personal stamp on plaque scoring, with the Turesky method being used in human teeth. The most accepted method in veterinary dentistry is the Logan and Boyce modification of the Turesky plaque index.

The Logan and Boyce modification of the Turesky plaque index is performed as follows. Plaque is disclosed with 2% erythrosin solution gently applied to the crown surface and immediately rinsed with water. The crown surface is horizontally divided into gingival and coronal halves, which are scored separately. Both coverage and thickness are assessed and given a numerical value based on the percentage surface coverage and thickness.

Coverage:

0 = No observable plaque

1 = Less than 25% coverage

2 = Between 25% and 50% coverage

3 = Between 50% and 75% coverage

4 = Between 75% and 100% coverage

Thickness:

1 = Light pink to light red

2 = Medium red

3 = Dark red

The score for each half of the tooth is calculated by multiplying the coverage and thickness scores. Gingival and coronal scores are added to give the total score for each tooth. The sum of the teeth scores are termed the whole mouth score and these are often multiplied by the number of animals in the study group and compared statistically to another group.

Calculus scoring

Calculus deposits can be grossly observed. No disclosing agents are used. A simple method can be used to score calculus in the clinic, based on coverage:

0 = No visible calculus

1 = Scattered calculus covering less than 25% of the buccal tooth surface

2 = Calculus covering between 25% and 50% of the buccal surface

3 = Calculus covering between 50% and 75% of the buccal surface

4 = Calculus covering between 75% and 100% of the buccal surface

For research studies and purposes, the Warrick Gorrel method is used. The final result is termed the calculus index.

The crown surface is vertically divided into mesial and distal halves, which are scored separately. Both coverage and thickness are assessed and given a numerical value based on the percentage surface coverage and thickness.

Coverage:

0 = No visible calculus

1 = Scattered calculus covering less than 25% of the buccal tooth surface

2 = Calculus covering between 25% and 50% of the buccal surface

3 = Calculus covering between 50% and 75% of the buccal surface

4 = Calculus covering between 75% and 100% of the buccal surface

Thickness:

1 = <0.5mm

2 = 0.5mm – <1mm

3 = >1mm

The score for each half of the tooth is calculated by multiplying the coverage and thickness scores. Mesial and distal scores are added to give the total score for each tooth. The sum of the teeth scores are termed the whole mouth score and these are often multiplied by the number of animals in the study group and compared statistically to another group.

Supra-gingival Scaling

Gross plaque and calculus deposits can be removed from the supra-gingival surfaces of the teeth with tartar removing forceps, hand-held scalers or power scalers. Hand-held scalers are instruments with a handle attached to a sickle shaped blade. Ultrasonic and subsonic scalers have been developed to decrease the manual energy required to remove plaque and calculus, to decrease fatigue of the operator’s hand and forearm and to decrease scaling time.

Removal of supra-gingival plaque and calculus is termed ‘scaling’.

Calculus removing forceps

Calculus removing forceps are designed in a similar fashion to extraction forceps, with the difference being they have one curved beak and one straight beak rather than two straight beaks. The straight beak is placed against the cusp of the tooth, whilst the curved beak is placed at the gingival margin. The handles are squeezed together which results in the calculus being chipped/shaved off. The force from the beaks is parallel to the long axis of the tooth, compared to extraction forceps, where the force would be across the tooth. Using calculus removing forceps, decreases the chances of fracturing the cusp.

The correct use of calculus removing forceps.

Hand scalers

Hand scalers have a handle connected to a blade, which has a double-sided cutting edge that converges to a sharp point. The blade is triangular in cross section. The sharp blade is used to remove plaque, calculus and other deposits from the supra-gingival tooth surface. They are held in a modified pen type grasp. The blade is placed on the tooth surface at the gingival margin and used in a pull stroke that moves the blade away from the gingival margin.

Hand scalers are also termed sickle scalers, based on their design and appearance. The most common are the Universal (or H6/H7), the Jacquette and the Morse. The Universal is the most common in Veterinary practices. The Universal has a long blade, the Jacquette has a medium sized blade and the Morse have small, almost miniature size blades. In an ideal world we would have every type and adapt the blade to the tooth. In the real veterinary world, the Universal will do an adequate job for all canine teeth, whilst the Morse can be useful for some of the smaller feline teeth. In some older veterinary practices, hoes and files are commonly used. Hoes are flat blades bent at 99 degrees to the handle. The hoe is placed on the tooth surface at the gingival margin and used with a pull stroke, similar to using a garden hoe in your vegetable patch! The most common hoe is called the McCall. Files should not be used to remove calculus from the tooth surface as they tend to gouge and damage the enamel, which promotes rapid plaque and calculus re-attachment after cleaning. Gouging and damage to the enamel cannot be repaired by polishing alone.

A curved scaler (A Universal – H 6/7).

A short blade scaler (Morse).

Ultrasonic scalers

Ultra-sonic scalers may be used for removal of supra-gingival plaque and calculus. Ultrasonic scalers operate at >25kHz. The principle action of plaque and calculus removal is either by a mechanical action or cavitation. The mechanical action is achieved by the vibrating tip contacting the calculus and breaking it off. Cavitation is the production of sound waves derived from physical vibrations of the tip energizing the water spray, which then clean the tooth. The cavitation effect can be dangerous to the operator. Cavitation produces a bacteria laden aerosol that when inspired by the operator may result in a respiratory infection.

Ultrasonic scalers run via electricity and the working tip has one of three types of movement. The magneto-strictive type utilize a stack of parallel nickel strips that lengthen and shorten when subjected to alternating electrical current. This causes the tip of the scaler to move in an elliptical figure of 8 motion. There are two classes of stacks, one vibrates at 25kHz, the other at 30 kHz. The piezo electric type scaler utilize a crystal in the handle that expands and contracts when subject to alternating current. This causes the scaler tip to move in a linear back and forth motion. It vibrates at 25 to 45 kHz. The ferric rod type scalers use a rod, which vibrates by expansion and contraction. This causes the titanium scaler tip moves in a circular or elliptical fashion. The ferric rods vibrate at 42 kHz.

The handle of the ultrasonic scaler is held in a pen-like grip. The tip is placed against the tooth surface at the gingival margin and in light contact with the calculus. The tip is moved using light strokes over the surface of the tooth. The operator should allow the vibrations to shatter the calculus. If the tip is used like a hand-held scaler, and force is placed against the calculus, the tip is likely to break. The ultrasonic scaler can be safely used on any tooth surface that you can visualize. The tip of the magneto-strictive scaler can get quite hot without adequate water cooling, to the point where damage to the tooth and surrounding tissues occurs. If the water-cooling is adequate to the tip, the ultrasound can be used to scale the gingival sulcus.

Acteon Satelec P5 ultrasonic scaler.

Using a magneto-strictive ultrasonic scaler to clean the maxillary 4^th premolar tooth. Note the water adjacent to the scaler tip.

Care must be used if the ultrasonic is used for sub-gingival pockets, as it is easy to overheat the epithelial tissues and the tooth. In time the dentine temperature may rise and result in pulpitis. The water spray should be directed at the end of the tip to dissipate heat. If used inappropriately or for excessive amounts of time on a single tooth or on young growing tissue, damage will result, so magneto-strictive and piezo type scales should not be used on puppies and kittens under a year of age. To avoid excessive heating of an individual tooth and tissue damage, the tip should be continuously moved over the tooth surface and a single tooth should only be scaled for a maximum 10 seconds at a time. If the ultrasonic scaler does not remove the calculus from the developmental ridges and cusps, then a hand-held scaler should be employed.

Sonic scalers

Sonic scalers work using high-pressure air from a compressor or air cylinder. The sonic scaler has a working tip that vibrates at 18-20 kHz and produces little heat as compared to the ultrasonic scaler. They usually have a jet of water spray for cooling the tooth and flushing away debris. The advantage is the reduced harm to the tooth via overheating or frequency of tip vibrations, but they can be slower with heavy calculus build-up. The Titan-S and NSK range of sonic scalers though do a similar job to any of the ultrasonic scalers on the market.

Roto-sonic scalers

Roto-sonic scaling burs (Roto-pro bur) have been used in some veterinary practices for a number of years. Actually the first practice I worked in had one of these. The roto-sonic scalers are 6 sided burs that fit into the high-speed air driven hand-piece. The principle is the bur spins at 300,000 rpm, has six sides, which equates to 1,800,000 sides/minute. Divide by 60 seconds, producing the equivalent power of 30,000 Hz or 30 kHz, equal to the ultrasonic scalers. The Roto-pro bur is a very effective means of removing calculus and plaque. It must be used with a very light touch though, as it removes the enamel as quickly as the calculus. The majority of veterinary dentists do not recommend its use. I would not use it to scale plaque and calculus as there are safer methods.

The appearance of the roto-sonic scaler against a maxillary canine tooth.

Sub-gingival Scaling (Root Planing) and curettage

While scaling only the tooth crown may be an aesthetic result for the owner, it does not really aid in the treatment of periodontal disease nor help with future prevention of periodontal disease. Complete treatment of established periodontal disease requires sub-gingival scaling and curettage. The term root planing is used to describe scaling of the tooth root. The act of root planing removes plaque, calculus and other foreign matter, i.e. hair, food, from the periodontal pocket, as well as, the superficial layer of endotoxin rich cementum from the root surfaces. The term gingival curettage is used to describe the action of scraping the necrotic epithelial cells, endotoxins and accumulations from the epithelial wall lining the pocket.

Root planing and sub-gingival curettage can be performed using ultrasonic and subsonic scalers or hand instruments termed curettes. Care must be used if an ultrasonic scaler is used in sub-gingival pockets, as they may overheat the epithelial tissues and the tooth. An increase in dentine temperature may result in irreversible pulpitis. To avoid or decrease damage and reduce the ultrasonic scaler heat, the water spray must exit from the tip for sub-gingival work. Ultrasonic scalers should not be used on bone, as necrosis will result. The ideal power scalers for sub-gingival work are the Acteon P5, 42-12 ultrasonic scaler and sonic scalers as they produce very little heat as compared to the magneto-strictive and piezo type ultrasonic scalers.

Traditionally, human dentists have used hand instruments for root planning and sub-gingival curettage. There are two types of curettes, the Universal and the area-specific. The Universal type, which Columbia and Barnhart are examples, have two cutting surfaces, a rounded toe and a blade with cutting surfaces angled at 90 degrees to the handle. The area-specific type, which Gracey is an example, has a rounded toe and a single sided cutting blade, which is angled at 70 degrees to the shaft (which is the part of the instrument between the cutting blade and the handle). I believe that Gracey curettes are the best for sub-gingival scaling and curettage as they adapt to the anatomy of our patients’ tooth roots.

The curette is held in a modified pen grasp. The curette is introduced into the periodontal pocket. When the blade reaches the base of the pocket, it is turned to contact the tooth surface. The shank of the instrument should be parallel to the long axis of the tooth for perfect contact of the blade against the root. Both types of curettes are used with a pull stroke from the depth of the periodontal pocket, with the blade against the tooth root surface. I have found that a minimum of 10 strokes are needed to adequately scale any one surface. Once calculus, plaque, hair, debris, food, diseased cementum, cementum endotoxins, necrotic and diseased cells have been removed from the pocket, a smooth, glass like sheen should be present on the tooth root. A clean pocket promotes reattachment of the epithelial wall to the tooth root via fibroblastic activity through production of collagen and connective tissues. Local delivery antibiotics, using doxycycline, can be used to enhance this action.

The introduction of a curette sub-gingivally.

There have been reports that ultrasonic and sonic scalers are as effective in removing sub-gingival accumulations as hand instruments, but I have not found this to be the case. In practical wet labs attended by veterinary students and Veterinarians, I have found that root planing is performed more thoroughly using sharp hand instruments. It has been reported that curettes produce less inflammation and less disruption of the uppermost periodontal fibres. They smooth the tooth root and produce less stripping and gouging than powered instruments. Curettes also remove less tooth structure. I recommend that powered instruments can be used safely to 4-6mm but hand instruments should be used below this.

The graph below is a summary of a study I performed with 4^th year Vet students from Sydney University Veterinary teaching Hospital during practical classes. The purpose was to measure the amount of calculus on the tooth root following root planning. Data from each tooth was collated based on number of roots and depth of the periodontal pocket. Periodontal probing depths were measured around each tooth. The root surface was scaled using hand-held instruments. The teeth were extracted. The calculus still remaining on the root surface was calculated and based on the total root surface of the tooth, given a percentage score. This was put into graph form.

The data produced demonstrated that it was more difficult to clean deep periodontal pockets and multi-rooted teeth.

Graph showing the increase of calculus coverage following root planning with respect to the depth of the periodontal pocket and number of tooth roots.

Polishing

Polishing the tooth surface following scaling is performed to remove any microscopic plaque and calculus and to provide a smooth tooth surface that retards the re-attachment of plaque and calculus. Supra-gingival scaling and root planing, even when done correctly, will leave a roughened enamel surface that will encourage plaque reattachment. Polishing is performed by applying an abrasive paste in a cup to the tooth surface. Pressure on the cup will flare the edges, which can then be directed slightly under the gum, to polish sub-gingivally.

Generally speaking, there are two types of polishing actions. The traditional cup, which rotates continuously at 5,000 rpm and the newer type of cup with a reciprocating action, back and forward. The cups should not be applied to the tooth surface for greater than two seconds duration as the heat generated can cause an increase in dentine temperature and an irreversible pulpitis. Pastes are available in different flavours and grades. Bubblegum, Mint, Pina Colada and Banana are popular. Fine grades produce a smoother finish, whereas course grades will remove more enamel and produce a rougher surface. It is also possible to purchase paste in a multi-use jar or individual caplets. The same prophy cup should not be repeatedly dipped into the multi-use jar during teeth polishing, as it will become contaminated. The paste can be placed into separate dappen dishes for each patient. A new cup should be used for each patient.

Prophy paste in a single uni-dose cup.

A polishing cup on a slow speed motor for polishing.

Prophy paste in a multi-use jar.

Using a polishing cup and paste on the maxillary 4^th premolar tooth.

Sulcular Lavage

Sulcular lavage is the term used to describe flushing the gingival sulcus and periodontal pockets with saline, water or dilute chlorhexidine. This is performed after the teeth have been polished to remove any free-floating debris and polish.

Fluoride

The use of fluoride has been popular in human dentistry to remineralise enamel, reduce cavity formation and desensitise teeth after cleaning. In veterinary dentistry it is used to re-mineralise the enamel and to act as an anti-bacterial. Fluoride ions bind to calcium to form a CaF bond. Post cleaning 1.23% acidulated fluoride can be applied to the enamel and root surface to desensitize it. Acidulated fluoride is deactivated by water, so it shouldn’t be washed off. Stannous fluoride paste can also be used to desensitise sensitive root surfaces, but care must be taken if the animal swallows it due to the potential renal toxicity of the tin.

Fluoride foam placed on the teeth after polishing.

SANOS

SANOS is a liquid polyvinyl that is applied by a small brush directly to the gingival sulcus and margin post scaling and polishing. The sealant seals the gingival sulcus against penetration of plaque but still allows the transversing of sulcular fluid and oxygen. The sealant has VOHC approval for reduction in plaque and calculus accumulation.

Oravet

Oravet is a wax barrier sealant, which acts as a plaque preventative. It is applied to the tooth surface and gingiva following teeth cleaning. The tooth surface should be dry, by wiping away any saliva or water with a swab, prior to application. The wax can be applied with a prophy cup, the applicator gun or a gloved finger. This will be discussed in the homecare module.

The Oravet introduction kit comprising application kit, wax containing cartridges and take home kits.

Appearance of Oravet barrier sealant after smearing with finger.

Rejuvenation and regeneration products

If it is possible to clean a 4mm pocket in a dog or a 2mm pocket in a cat, shrinkage of the oedematous gum will occur and re-establishment of the normal gingival sulcus depth will result. When the pocket is greater than this, the pocket will accumulate plaque and food in a matter of days following cleaning. It is therefore important to fill the pocket with a product that will prevent this. Products that encourage reattachment of the gingiva to the tooth root, i.e. rejuvenation using Doxirobe and products that stimulate new periodontal ligament and alveolar bone, i.e. regeneration, using Synergy are encouraged to restore the periodontal tissues.

Doxirobe

Doxirobe is a doxycycline impregnated polylactic acid polymer gel. Following root planning, Doxirobe is placed into the periodontal pocket. Doxirobe gel polymerises on contact with water, saliva or blood. The gel adheres to the tooth root, as well as filling the void between the gingival margin and the tooth, thereby preventing plaque and debris entering the periodontal pocket. As the polylactic acid degrades, doxycycline is released, making it available for its antibacterial and anti-collagenase action. As an antibacterial, it is bacteriocidal against anaerobic periodontal pathogens for up to six weeks. Doxycycline also binds to the calcium in the tooth root and is subsequently released at anti-collagenase levels for up to nine months. Doxcycline binds to the collagenase enzyme, inhibiting collagen resorption and further loss of the periodontal ligament. Doxirobe also stimulates fibroblasts, which promotes reattachment of the epithelial pocket lining to the tooth root surface. Doxirobe can be used in any periodontal pocket.

Diagramatic demonstration of gel usage.

Demonstration of placing Doxirobe into periodontal pocket in a dog.

Synergy osteoconductive synthetic bone material

Synergy is an osteoconductive synthetic material, which can be used in periodontal pockets to promote new alveolar bone production and encourage re-attachment of the gingival tissues and periodontal ligament or into post-extraction sites to maintain bone density.

Synergy crystals are a mixture of tricalcium phosphate and hydroxyapatite.

Instrument sharpening

On my visits to veterinary clinics over the years, I have observed that hand instruments do not get sharpened, as often as they should, and therefore are blunt. It is mandatory that scalers and curettes are kept sharp. A blunt or dull blade will not remove accumulations and will burnish the calculus against the tooth root surface. Sharpening is a skill that takes time to master, and if one person in the clinic can sharpen well, your dentistry will improve.

Repeated use of scalers and curettes wears away the metal on the blade resulting in a dull, ineffective action. A sharpening stone should be used after each use. Stones come in all shapes and varieties. The Arkansas stone is a fine textured natural stone that will remove a small amount of the instrument metal producing a sharp edge. It can be used wet or dry. The courser stones, Aloxite or India, can be initially used on very dull instruments and then a final sharpening on an Arkansas stone for a sharp finish.

Each instrument requires sharpening at a different angle. The angle is measured from the sharpening stone to the handle of the instrument. The hand scaler has two edges. One side requires the handle to be parallel to the stone, whereas the opposite edge requires a 20-degree angle.

Gracey curettes have one edge that requires sharpening. In order to determine which side is the cutting surface, hold the curette handle vertically. The two sides of the blade will be obliquely angled to the horizontal, with the sharp edge being the lower of the two. The Gracey curette requires the cutting edge to be sharpened at angles of 110 degrees to the stone, but it is often easier to hold the handle at 45 degrees to the stone to achieve the same aim. If you sharpen your instruments, it takes 3-5 strokes to re-sharpen it. If you don’t, it takes ten strokes to sharpen a blunt instrument and 20-30 strokes for a very blunt instrument. Each instrument should be re-sharpened after every patient and then autoclaved. The sharp edge can be tested by drawing the blade along a piece of plastic, like a syringe case. If it is sharp, a curled piece of plastic is shaved, if it is blunt, no plastic is removed.

Demonstration of sharpening a hand instrument on a stone.

Handpiece Maintenance

All hand instruments, scalers, curettes and probes require cleaning and sterilising after each use.

At our practice, we scrub instruments with surgical disinfectant to remove gross contamination, place them in an ultrasonic bath to remove minute contamination and rust, followed by sharpening and autoclaving.

Problems with air-driven dental handpieces most often result from improper cleaning and lubrication. Following use, the high and slow speed handpieces should be thoroughly cleaned to remove any contamination including blood, saliva, tooth and soft tissues, etc. Inadequate cleaning of the handpiece before sterilisation can result in collection of debris in the internal parts of the handpiece. This creates wear similar to sludge within your car engine. The exterior of the handpieces can be cleaned with any good surgical disinfectant. Be sure to rinse and dry thoroughly.

The prophy cup should be disgarded from the slow speed handpieces and the bur in the high-speed handpieces should be replaced with a blank prior to lubricating and autoclaving. High-speed handpieces should not be run without a bur or blank in the head, as the turbine will be damaged. The handpiece should be lubricated with a dental lubricant. This can be achieved by placing a small squirt of lubricant into the 2nd largest hole at the base of the handpiece. The handpiece should be held upside down and run for 10 seconds.

It is advisable to remove the rubber washer at the base of each handpiece prior to autoclaving.

All instruments should be autoclaved prior to use on the next patient.

If a compressor is used to supply air to the handpieces, the valve should loosened and the compressed air released each day to prevent humidified oily air settling in the bottom of the tank. This will prevent rust forming in the tank.

References

1. Clinical Periodontology, ed. Carranza FA. 7^th ed. WB Saunders, Philadelphia
2. Small Animal Dentistry, ed. Harvey CE & Emily PP. 2^nd ed. Mosby, Baltimore
3. Veterinary Dentistry, ed. Wiggs RB & Lobprise HB. Lippincott-Raven, Philadlephia
4. Veterinary Dentistry for the General Practitioner, ed. Gorrel C, Saunders, London
5. Veterinary Dentistry, ed. Clarke DE, Clarke, Melbourne
6. Handbook of Small Animal Dentistry, eds. Emily PP & Penman S, Pergamon Press, Oxford
7. Periodontology, ed. Radeitschak KH, 2^nd ed. Thieme Medical Publishers, New York
8. Periodontitis in Man and Other Animals, ed. Page RC & Schroeder HE, Karger, Basel