PERIODONTITIS

Periodontal disease is the most common infectious disease in the world, affecting
over 85% of all dogs and cats over 2 years of age. The cause of periodontal disease
is PLAQUE. Plaque is primarily made up of bacteria.

Periodontal disease is a disease of the supporting structures of the teeth, the gums,
jawbone and periodontal ligament. Two major diseases make up periodontal disease.

Gingivitis is the first. It is completely reversible, and is recognized by the classic signs
of hyperplasia, oedema, haemorrhage and inflammation of the gums, oral pain on
chewing and home care, and halitosis.

Periodontitis is the second. It is irreversible and attacks the deeper structures that
support the tooth, permanently damaging the alveolar bone and periodontal ligament.
Periodontitis eventually results in tooth mobility and tooth loss.

Stages and Treatment of Periodontal Disease

First Stage = Gingivitis. Minimal plaque and calculus. Gingival inflammation, no

bleeding on probing, normal periodontal probing depths (PPD). Treatment includes
supra-gingival and sub-gingival scaling, polishing, irrigation and home care. Excellent
prognosis.

Second Stage = Advanced Gingivitis. Increased plaque and calculus. Gingival

oedema, bleeding on probing, normal PPD. Treatment includes supra-gingival scaling
and sub-gingival scaling, polishing, irrigation and home care. Good prognosis.

Third Stage = Established Periodontitis. Moderate plaque and calculus. Loss of

periodontal attachment levels (PAL) with moderate to deep pocket formation and up to
25% loss of alveolar bone. There may be tooth mobility. Treatment includes supra and
sub-gingival scaling (root planing and gingival curettage), antibiotic and analgesic
administration, polishing, irrigation, guided tissue rejuvenation or guided tissue
regeneration (Consil/membranes), possible extractions and home care. Guarded
prognosis without regenerative surgery.

Fourth Stage = Advanced Periodontitis. Large deposits of plaque and calculus,

especially subgingivally. There is advanced breakdown of the supporting tissues of
the teeth with severe increases in pocket depth (greater than 25% attachment loss) or
severe gingival recession. The tooth is very mobile or may have fallen out. Treatment
includes supra-gingival and sub-gingival scaling, (root planing and sub-gingival
curettage), polishing, irrigation, and advanced gum flap surgery, guided tissue
rejuvenation or guided tissue regenerative surgery (Consil/membranes), extractions
and home care. Poor prognosis without guided tissue regenerative surgery.

AETIOLOGY

Tooth surfaces are first covered by the dental pellicle, an acellular layer of salivary
and alimentary glycoproteins, polypeptides and lipids.

Plaque formation involves the adherence of bacteria to the pellicle and proliferation of
these bacteria supragingivally, which are initially dominated by Actinomyces viscosus
and Streptococcus sanguis.
With supragingival plaque development, gingivitis develops, and the plaque extends
subgingivally. Aerobes consume the oxygen beneath the gum, creating a more
suitable environment for anaerobic bacteria to establish themselves.

With the development of a subgingival bacterial population and the developing

inflammation, periodontitis occurs. The main anaerobic bacteria responsible are:
Porphyromonas spp. (previously black-pigmented Bacteroides), Prevotella spp.,
Peptostreptococcus spp., Fusobacterium spp. and the Spirochetes. Anaerobes
constitute 25% of sub-gingival flora in dogs with healthy gingiva and 95% in dogs with
periodontitis. Inorganic substances from saliva, mainly calcium, carbonates and
phosphorus are deposited onto plaque to form calculus. The calculus has a very
rough surface, which is ideal for further plaque attachment.

PATHOGENESIS

Supragingival bacteria at the gingival margin and subgingival plaque within the sulcus
produce inflammation of the free and attached gingiva. Proliferation of subgingival
bacteria induces a destruction, and apical migration of the epithelial attachment. If no
gingival recession occurs, a periodontal pocket is formed. This enables more plaque
to enter the pocket and further tissue damage occurs. This becomes a progressive
disease.

Initially, the body’s defense mechanisms are activated, with plasma factors such as
complement flooding the gingival fluid. This produces an inflammatory reaction. If this
fails, the host defense floods the gingival sulcus with neutrophils. If they cannot
control the bacteria, then the development of plasma cells and lymphocytes are
brought into the area. During advanced periodontitis, tissue damage results from
bacteria, bacterial by-products and from the chronic inflammatory reaction. There is
now strong evidence that anaerobic bacteria are only the initiating cause of
periodontal disease, and it is the host’s own inflammatory reaction that continues to
fuel the inflammation.

Because the periodontal pocket is a semi-permeable membrane, there is a constant

stream of inflammatory mediators and bacteria entering the gingival tissue, and thus,
the systemic circulation. This in turn, results in a generalized infection and possibly
future endocarditis, glomerulonephritis and meningitis, which have all been reported in
the human literature.

Once the inflammation extends into the periodontal pocket, Bacteroides spp. and
macrophages release collagenases, which are able to degrade collagen. Perivascular
collagen is the first to be lost, but as the periodontal ligament is reached, this too, is
lost, as it is 90% Type 1 collagen. As the disease advances into the developing
periodontal pocket, and the inflammation reaches within 2mm of the alveolar bone,
bone loss occurs. The bone loss is associated with a shift in the bone resorption and
bone formation process in which local cytokines are released from chronic
inflammatory cells. The inflammatory cells are generated by the presence of plaque
and the subsequent host response to the plaque microflora. There are many
inflammatory mediators involved, one of the cytokines that has received intense
interest, in relation to its effect on bone resorption, is interleukin-1 (IL-1). IL-1
stimulates both mature osteoclasts and the proliferation of osteoclast precursors.

It also appears, that in part the resorption is related to prostaglandin (PG) release,
because indomethacin partially inhibits the bone resorption. Chronic inflammatory
cells release both PGs and leukotrienes (LT). In several studies PGE levels are
increased in cervicular fluid from periodontal sites, which resolve once the disease is
treated. Another study by Williams showed that fluriprofen reduced bone loss in
periodontitis patients. These sugest a critical role for qarachidonic acid metabolites in
the bone resorption found in periodontal disease. More importantly, they
demonstrated the significance of the host response in the pathogenesis of periodontal
disease. The bone and periodontal ligament like to be at least 1mm from the
advancing inflammation, thus the disease continues down the tooth root until there is
no support and the tooth falls out.

In reality, it is not as simple as this, as the advancing disease is halted by the immune
system every now and again, and periodontal disease is actually a disease of
quiescence with random bursts of activity.

Treatment can halt and even repair the damage done in many cases, by the use of
proper cleaning, antibiotics and anti-inflammatory drugs.

VETERINARY CARE

The veterinary treatment of periodontal disease involves the mechanical removal of

plaque and calculus with the patient under general anaesthesia. The methods include
tooth scaling, root planing, polishing and periodontal sulcus/pocket recording and
charting.

THE DENTAL CLEAN (PROPHYLAXIS)

1. Pre General Anaesthetic check and Oral Examination

2. Administration of antibiotics, anti-inflammatories, analgesics
3. General Anaesthesia
4. Operator Protection (Mask, Gloves, Face Shield)
5. Periodontal Probing and Recording (Charting)
6. Gross removal of supra-gingival plaque and calculus
7. Sub-gingival scaling (root planing and sub-gingival curettage)
8. Polishing
9. Sulcular Irrigation
10. Extractions or guided tissue rejuvenation/regeneration
11. Radiology
12. Home Care Instructions

THE PROPHY KIT

1. Periodontal probe
2. Explorer
3. Dental Mirror
4. Supra-gingival scaler (H6/7, Jacquette)
5. Subgingival curettes (Gracey/Barnhart/Columbia)
6. Elevators (Apical 301, winged #1-4)
7. Root tip pick
8. Extraction forceps
9. Tartar removing forceps
10. Minnesota retractor
11. Periosteal elevator, scalpel blade, sutures
12. Rejuvenation products (Doxirobe), Regeneration products (Consil/membranes)
13. Antibiotics and anti-inflammatories (NSAIDs)

Anaesthesia

The animal should have an endotracheal tube placed due to the water and aerosols
produced, and the pharynx should be packed with bandage. The operator should
wear glasses to protect the eyes from flying tartar and a mask to prevent inhalation of
the bacterial laden aerosols.
Antibiotics and pain relief.

There is mounting evidence that scaling of the dirty tooth surface cannot be done with
100% efficiency, and that a small amount of calculus and plaque is left on the root or
in the furcation irrelevant of how experienced the operator is. For this reason,
antibiotics pre-anaesthetic/dental are sometimes recommended whenever a
periodontal pocket will be encountered. The most effective antibiotics for dental use
are clindamycin, doxycycline and metronidazole. Clindamycin can be given at
5.5mg/kg BID for gingivitis and 11mg/kg BID for osteomyelitis. Clindamycin is able to
penetrate the biofilm layer of the plaque. Doxycycline can be given at 2.5 – 5.0 mg/kg
sid-bid, inhibits collagenase, is antibacterial, as well as having anti-inflammatory
properties, even at sub-microbiological levels. Metronidazole is used for anaerobic
infections at 15mg/kg bid or 30mg/sid.

Dentistry by definition produces pain, whether it be during root planing, finding a

fractured tooth, or doing an extraction. Pre-anaesthetic pain relief can be achieved
with either opioids, NSAIDs, peri-operative local anaesthetics and regional nerve
blocks.

Probing and Charting

A graduated periodontal probe is placed under the gingival margin to determine the
depth of the gingival sulcus. This examines the true damage and allows a yardstick for
future measurement. The depth of the gum pocket is measured in millimetres from the
edge of the gum along the root surface towards the root tip. With healthy gums, the
pocket measurement should be 0 - 0.5mm and 2 - 3 mm in the cat and dog
respectively. Measurements of 1mm or greater in cats and 4mm in dogs indicate
disease. Once disease is present, radiographs and gum surgery may be necessary.
These measurements and any other abnormalities are recorded on a chart for future
reference.

Supragingival Scaling

Once the dog is anaesthetised, the plaque and calculus is removed by mechanical
‘scaling’, using an ultrasonic scaler, subsonic scaler or hand instruments to remove
calculus from above the gumline.

Ultra-sonic scalers are powered directly with electricity and generate 25-40 kHz at the
working tip. They create a large amount of heat and need to be water-cooled. The tip
should only be left against the tooth surface for 5 seconds at a time. There are
different tips and this should be considered when using them, as the piezo-electric tip
vibrate back and forth and the tip should not be used directly against the tooth
surface. The magneto-strictive and sonic scalers vibrate in an elliptical way and either
the tip or side can be used.

Air driven dental units use high pressure from an air compressor, or compressed
air/nitrogen to run high-speed handpieces and a subsonic scaler. The scaler has a
working tip that vibrates at 15-20 kHz to shatter the tartar from the tooth surface and a
jet of water spray for cooling the tooth and flushing away debris. The side of the tip
should be used with gentle brush strokes over the whole surface of the crown.

The high-speed handpiece spins at 400,000 rpm, is equipped with water coolant and
can be purchased with a fibre optic light source. The high-speed drill is used to
section teeth before extraction or make access openings in the enamel for root canal
work. The handpiece takes friction grip burs, usually round or tapered fissure in
shape, and either diamond or tungsten carbide cutting edges.
The roto-sonic scalers are 6 sided burs that fit into the high-speed air driven
handpiece and when rotated at 300,000 rpm, set up an effect that dislodges the
calculus from the enamel. The rotopro bur must be used with a light touch as it may
remove the hard enamel layer.

The slow speed handpiece can be used for polishing or cutting of dentine, and take
right or contra angle burs and polishing cups.

Supragingival calculus can also be removed using hand scalers. Scalers have a
triangular shaped blade with a double-sided cutting edge; they should be regularly
sharpened, and best not used below the gumline. They are held in a modified pen
type grasp. They are placed at the gum edge, and are moved away from the gum so
taking the calculus with the blade.

Sub-gingival Scaling and Root Planing

After supra-gingival scaling is complete, sub-gingival calculus can be removed using a

curette. This is termed root planing and gingival curettage. Root planing also helps to
remove the superficial layer of endotoxin rich cementum from the root surfaces, thus
providing a smooth root surface for quicker epithelial reattachment.

Gracey curettes have a rounded toe and a single cutting edge. The most common
Gracey curettes are used in a pull stroke from the depth of the periodontal pocket,
with the blade against the tooth root surface and the handle at 45-90 degrees to the
long axis of the tooth. About 10-20 strokes may be required to dislodge calculus on
any one surface. This smoothes the root to allow reattachment of connective tissue,
removes calculus and bacterial endotoxins. The curette is held in a modified pen
grasp.

Periodontal disease will continue if calculus is not removed from under the gum. The
practice of removing calculus from only above the gum does nothing in the prevention,
or halting the advancement, of periodontal disease.

Polishing

Scaling, even when done correctly, will produce a rough tooth surface that will
encourage plaque reattachment. Applying a mild abrasive paste in a slowly rotating
cup to the tooth surface performs polishing. Excessive force or time should not be
used as the heat generated may damage the pulp. The cup edges should be flared
slightly under the gum, to polish subgingivally.

Sulcular Lavage

Sulcular lavage involves flushing the gingival sulcus and periodontal pockets with
saline or dilute chlorhexidine to remove any free-floating debris. This should be
performed after the teeth have been polished.

Gingival Surgery and rejuvenation/regeneration

In pockets greater than 4mm, it is difficult to ensure all subgingival deposits have been
removed. A gingival flap may be raised which allows direct access and visualisation.
Otherwise, extraction may be considered for some of these situations.

If it is possible to clean a 4mm pocket, you should get reduction of the oedematous
gum and re-establishment of the normal periodontal sulcus depth. When the pocket is
greater than 4mm, a clean pocket will fill up with plaque and food in a matter of days,
it is therefore important to fill the pocket up with a product that will prevent this, as well
as encourage reattachment of the gum to the tooth root.

Consil is a bioglass, which is osteoconductive. It therefore promotes new alveolar

bone growth and can be used in extraction sites or in deep periodontal pockets to
encourage new attachment of the gingival tissue, new bone and periodontal ligament
growth and re-establishment of the attachment apparatus. It hardens on contact with
blood, but because it has the consistency of sand, the gingival must be closely
attached to the tooth or it will all fall out.

If these tissue rejuvenation or regeneration techniques fail, then a gingival tissue flap
can be repositioned, either apically or laterally. If the disease involves a periodontal
pocket, an apically repositioned flap can be considered. This involves making two
parallel vertical incisions either side of the pocket and repositioning and suturing the
gingival margin at a lower height, thus artificially reducing the depth of the periodontal
pocket. If gingival recession is involved, a lateral sliding gingival flap can be
considered. This involves making a vertical incision lateral to the defect to produce a
piece of gingival tissue that can be slid laterally to cover the defect and sutured.
These techniques are well covered in any of the human or veterinary periodontal
texts.