Periodontal disease (Gum disease, gingivitis, periodontitis)

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• Disease of supporting structures of teeth, ie gingiva, alveolar bone and periodontal ligament.
• Common incidental finding during routine clinical examination, eg at vaccination, or annual wellness examination.
• Cause: mainly bacterial plaque on teeth.
• Signs: minimal until disease is severe; halitosis, dysphagia (especially hard food), hypersalivation, rubbing mouth on ground or with paws, general malaise.
• Treatment: scale/polish, selective extraction, effective home care.
• Diagnosis: (minimal until disease is severe) halitosis, dysphagia (especially hard food), hypersalivation (possibly with blood streaks from bleeding gums), rubbing mouth on ground or with paws, general malaise.
• Prognosis: depends on owner compliance.
• Prevention: gradually change to dry food diet.
   Print off the Owner Fact sheets on dental disease in your cat and Periodontal disease and how to prevent it  to give to your client.

• Halitosis.

• Dysphagia.
• Hypersalivation, sometimes with blood.
• Oral discomfort .
• Renal, cardiac, hepatic, pulmonary, brain disease due to hematogenous bacteremia from periodontal lesions.

• Developed countries where processed food forms main part of diet.

• Old.

• 3 years (85% of all cases).

• 2-3 years.

• 0-1 year.

• Periodontal surgery.
• Reduced value of show animal.

• Scale/polish + subgingival scaling + selective extractions.

• Prevention by change to dry diet + effective home care (difficult in most cats).
• Effective home care:
  • Daily plaque removal (brushing).
  • Dental exercise (chew toys).
  • Regular oral exams.

• Age.
• Possible concurrent renal, cardiac, hepatic insufficiency due to periodontal-induced bacteremia.
• Aspiration of oral fluids - if cuffed endotracheal tube or throat pack not used.

Concurrent aseptic surgery

• Wound contamination by massive bacteremia/bacteria-laden spray produced by dental scaling, eg if operating on same animal or other animals in same air space.

• Bacterial plaque increased by processed food diet, poor immune status.

• Processed food diet because more likely to stick to teeth and impede immune system.
• Lack of effective home care when on processed food diet.

• Overcrowded and rotated teeth.
• Malocclusion.
• Retained temporary teeth.
• Slab fractures of teeth exposing rough dentine surface.

• Trauma.

• Chemical irritants.
• Systemic disease.
• Decreased flow or production of saliva, eg open-mouthed breathing, which dehydrates and thickens saliva, decreasing its defensive ability.

• Existing calculus (mineralized plaque) with rough surface aiding accumulation of more plaque.

• Dental plaque microbes or leucocyte response proteases, collagenases and elastases break down the periodontal tissue inflammation and destruction.
• Changed balance between omnipresent oral bacteria and animal's defense mechanisms in favor of bacteria.
• Bacteria adhere to pellicle and are allowed to accumulate in a matrix of salivary glycoproteins and extracellular polysaccharides, thus forming plaque.

• Oral bacteria sticks to pellicle (thin protein layer coating all exposed tooth surfaces) forms supragingival plaque (non-motile, aerobic, gram-positive cocci and rods) mineralized plaque (calculus), firstly on upper carnassial due to proximity to parotid duct of mineral-rich saliva.
• Normal: animal's natural defense mechanisms protect underlying tissues from bacterial invasion.
• Pathological: inadequate natural defense mechanisms and immune status plaque bacteria proliferate and accumulate inflamed line along gingival margin/interface with tooth (marginal gingivitis, first stage of reversible periodontal disease) reversible by effective home care if none or ineffective home care increasingly thick plaque layer bacterial population changes to include anaerobic, motile, gram-negative rods and filamentous organisms with greater tissue destructive properties gingivae become swollen and edematous, opening up gingival crevice subgingival plaque develops worsening gingivitis with gingivae bleeding when touched.
• Even severe gingivitis is reversible with a thorough scale and polish followed by effective home care.
• Gingival hyperplasia may develop.
• Epithelial attachment recedes apically (towards tooth root); gingival margin may also recede, exposing tooth root surface, or it may remain in its normal position (or recede more slowly than the epithelial attachment) producing a pocket; first stage of irreversible periodontitis.
• Bacterial endotoxins and tissue response result in rapid progression of disease process.
• Periodontal ligament and alveolar bone progressively destroyed as epithelial attachment recedes.
• If full thickness of alveolar bone destroyed = horizontal bone loss; epithelial attachment usually remains coronal to remaining alveolar bone = suprabony pocket; often gingival margin recedes with epithelial attachment = periodontitis without pocket formation.
• If partial thickness of alveolar bone destroyed = vertical bone loss; epithelial attachment often recedes apically beyond crest of remaining alveolar bone = infrabony pocket; rapid progression to deep pockets, often exuding pus.
• Tooth becomes mobile once over 50% periodontium destroyed, further weakening remaining periodontal ligament.
• Tooth exfoliated, taking majority of bacteria with it.
• Socket heals and slowly fills with sclerotic bone (3-6 months).

• Variable and largely dependent on presence of predisposing factors.
• May progress from gingivitis to periodontitis in a week or may remain as gingivitis, depending on immune status of animal + predisposing factors.

• Halitosis.

• Halitosis.

• Hypersalivation.
• Dysphagia.
• Oral discomfort.
• Blood-streaked saliva.
• Generalized malaise.

• Halitosis.
• Inflamed gingivae - bleed easily .
• Dental plaque/calculus.

• Periodontal pockets/abscesses .

• Gingival recession.
• Systemic disease via hematogenous spread of bacteria from mouth to heart, kidneys, liver, lungs.
• One or more loose teeth .
• Excess saliva, often thick, sometimes with bloodstreaks.

• Periodontitis, not gingivitis; identification of exact tooth involvement and degree of bone loss.

Serology

• Check FeLV and FIV status if suspect immunocompromized.

• Clinical signs.
• History.

• Radiography.

• Renal failure may be suggested by uremic smell and smell from oral uremic ulcers.
• Respiratory disease.
• Immune deficiency disease.

• Remove gross calculus + prophylactic antibiosis, eg amoxycillin , clindamycin , to decrease oral bacterial load and hence bacteremia and bacterial aerosol production during subsequent scaling.

• Dental scaling .

• Effective home care: ideally daily tooth brushing if mild gingivitis, some plaque and no calculus (difficult in cats).

• Palliative anti-infective agents, eg slow release oral pads, impregnated chews, oral gels, antibiotics.
   May be temporary improvement while used but recurrence afterwards if debris and plaque still present.
   Debris and plaque accumulations must be physically removed.

• Plaque accumulation: use disclosing solution (erythrocin food coloring) applied to teeth of conscious cat then rinsed off plaque retains dye can advise owner which areas not being cleaned effectively by them.
• Halitosis: indicates return of periodontal disease or presence of, for example, respiratory tract or renal disease.
• Gingivitis: suggests recurrence of plaque, eg due to poor home care +/- immune deficiency disease.

• 2-4 days post-operative check: discuss home care. Mouth should have recovered. Owners should now be brushing all teeth daily, having started on canine and incisor teeth for first 2 days.
• 2 weeks post-operative check: discuss home care; check amount of plaque recurrence using disclosing solution and modify home care accordingly.
• 2 months post-operative check: as above.
• Every 3-6 months: depending on condition, owner compliance and ability: as above.
   Set up dental health clinics (preferably free), which can be run by a specifically trained nurse, to encourage clients to return. Sales of toothpaste, toothbrushes, dietary supplements, dental operations and other items will provide a profit.

• Improve immune status by improving diet: raw meat or dry diet.
• Reduce plaque build-up: improve diet/physical cleaning.

 Effective home care is essential to prevent recurrence.

• Dry diet.
• Live enzyme supplement.
• Cat toothpaste/brush.
• Raw food diet may be beneficial.

• Poor if irritants not removed and mouth not cleaned.
• If no effective home care, oral health will return to pre-operative state in 2-8 weeks.
   Remember risk of hematogenous spread from reservoir of infection in mouth to kidneys, heart, liver and lungs, and perform appropriate tests to assess functioning of these organs as necessary.

• Absence of halitosis and recovery of gingivae within 2-3 days after scale and polish.

• Poor operative procedure, eg debris remaining subgingivally, careless use of scalers, no polishing.
• Poor home care, either from lack of owner compliance or from lack of proper advice and demonstration from the veterinarian.
• Non-diagnosis of other disease processes, eg renal insufficiency.

• Recent references from PubMed.
• Gorrel C (1998) Periodontal disease and diet in domestic pets. J Nutr 128, 2712S-2714S.
• Lonsdale T (1995) Periodontal disease and leucopenia. JSAP 36, 542-546. (Interesting information on relationship between raw food diet and dental disease.)

• Dr Mark Thompson DVM DipABVP, 179 Island Ford Road, Brevard, NC 28712, USA.

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