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Subgingival Scaling and Local Delivery System Perioceuticals
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.
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.
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.
With supra-gingival plaque formation, and contact with the free gingival, 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 fourth premolar 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.
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 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.
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.
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 a dog.
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.
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.
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. It can be separated into various stages based on presention:
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.
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 rationale for treatment is:
- Removes plaque and calculus from the tooth surface
- Removes diseased cementum and endotoxins on root surface
- Decreases the quantity of bacteria present on the tooth surface and in the periodontal pocket
- Provides a smooth tooth and root surface that decreases rate of plaque re-attachment
- Provides a clean root surface for pocket epithelium reattachment
- Provides a clean tooth surface which the owner can keep clean
- Relieves pain and inflammation
- 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.
The first step is to have the correct equipment and in order to improve scaling and polishing the procedure is to perform a thorough dental examination, probing and charting.
Probing and Charting
Periodontal probes are used to determine the position of epithelial attachment and thereby measure the depth of the gingival sulcus and periodontal pockets. 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. The depth, if abnormal is then recorded on the dental chart (attached).
Diagram of ‘how to use a periodontal probe’.
Placement of the periodontal probe to measure periodontal pocket depth of 10mm of the mandibular 3rd incisor tooth.
Each of the probing depths are placed on the chart adjacent to the tooth, ie 6mm pocket on buccal surface of maxillary left canine tooth; 8mm pocket on bccal surface of mandibular left 1st molar tooth.
Any pathology is also recorded on the dental chart. Below is a copy of our clinic’s charts and ‘Betty Edmunds’ pathology is recorded on the chart, ie The maxillary right 4th premolar tooth was fractured and required a root canal treatment to be performed – represented by a # symbol and filled in ‘lollipop’; there was a supernumerary maxillary right 3rd incisor requiring extraction – represented by a cross in a circle; also extracted were the maxillary left 2nd and 4th premolars and mandibular right 1st molar – represented by crosses over the tooth; the mandibular left 2nd incisor and 3rd premolar were missing – represented by a circle around the tooth. The other pathology symbols are in the Abbreviation key text box on the left side of the chart.
Plaque and calculus may also be recorded on the chart. These can be designated an index from 0 to 4 which represents the degree of gingivitis of the gum and the amount of calculus on the tooth surface as per the chart box. The number index and number are then recorded on teh chart.
Sub-gingival Scaling (Root Planing) 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 ultrasonic scaler with the curette shaped blade as they produce very little heat as compared to the standard 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 blade of a Gracey curette.
The curette is held in a modified pen grasp.
Closed root planing is performed when the curetted is placed into the periodontal pocket and the operator is doing the procedure blind. 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 can be used to enhance this action.
The introduction of a curette sub-gingivally.
Diagram showing the steps of root planing.
Closed root planing is performed by the elevation of a gingival flap and debridement of the root surface under direct vision. In this case, vertical incisions are made through teh gingiva and/or mucosa, raise the flap to visualise the root surface and proceed as described above. At teh end, the flap is placed back over the root with or without medications and sutured to the adjacent healthy tissue. If teh root is a single walled pocket then gel may be used, if the furcation is exposed, the a bone graft may be used.
Incision prior to open root planing.
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 4th 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.
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 local delivery antibiotics and products that stimulate new periodontal ligament and alveolar bone, i.e. regeneration, using Consil are encouraged to restore the periodontal tissues.
Local delivery antibiotic system
Doxycycline impregnated polylactic acid polymer gel or pluronic gel may be used to 1. Fill the void created by the loss of epithelial attachment, and 2. Stimulate fibroblasts to produce new tissue to re-attach the epithelial wall to the cementum/dentin of the tooth. This is more correctly termed rejuvenation rather than regeneration, as periodontal tissue and alveolar bone is not produced. Following root planning, so that the necrotic epithelial cells and the diseased cementum are removed, the antibiotic impregnated gel is placed into the periodontal pocket. Polylactic acid polymerises on contact with water, saliva or blood whereas pluronic gel hardens on temperature rise. The gel also 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 gel degrades slowly over time, the antibiotic is released, making it available for its antibacterial and anti-collagenase action. As an antibacterial, doxycycline is bacteriocidal against anaerobic periodontal pathogens for up to six weeks. Doxycycline also binds to the calcium in the cementum/dentin 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. Doxycycline has a 78-80% susceptability against anaerobes and can also be given if systemic antibiotics have been prescribed.
The gel and antibiotic is provided in two separate syringes, which must be joined and activated prior to usage. Once mixed, a catheter is placed onto the syringe, which is then placed subgingivally to the base of the pocket. The gel is then slowly injected whilst the catheter is withdrawn. The gel should be finished just short of the gingival margin so chewing doesn’t remove it. Every two weeks, the pet can be brought back to the surgery and a probe placed to confirm whether 1. The gel is still in palce, and 2. If the pocket is shallower. If the gel has been lost or normal periodontal probing depths have not been achieved, then it can be replaced in the consulting room awake or under sedation. This is repeated until normal probing depth is achieved.
Synergy is a hydroxyapatite / beta tricalcium phosphate particle osteoconductive / osteoinductive synthetic bone particulate, which can be used in periodontal pockets and furcations to promote new alveolar bone production and encourage re-placement of the periodontal tissues and alveolar bone. Synergy has the consistency of sand. Again, following subgingival curettage, +/- raising a gingival flap, the Synergy is placed around the tooth root. I receommend to fill the pocket to 2mm short of the gingival margin and then placed interdental sutures to prevent loss of the product. Radiographs can be taken to confirm placement and then in 3 months to confirm alveolar bone and re-attachment of the periodontal ligament using a probe. In the maxilla, Synergy can be difficult to keep in situ, so the gingiva must be closely attached to the tooth using purse-string sutures or a small amount of Super Glue along the gingival margin.