Periodontal disease, similar to most other diseases, should be treated as soon as it is diagnosed. The more important questions become:

 When is periodontal inflammation disease?

 What is the appropriate treatment for the severity of the condition?

Introduction

Cementum covers the dentine of the root similar to the way that enamel covers the crown. The gingival epithelium attaches to the tooth at or slightly below the cementoenamel junction (CEJ) where it protects the periodontal ligament (PDL), cementum and bone from the environment of the oral cavity. The PDL attaches the cementum to the alveolar bone ('socket'). Periodontal disease classically refers to inflammation or disease of any tissues of the periodontium, including the gingiva, cementum, PDL and alveolar bone. The space between the tooth and free (marginal, unattached) gingiva is the gingival sulcus, and is normally less than 3 mm deep in dogs and 0.5 mm in cats.

Gingivitis is the result of bacterial plaque accumulation and the associated inflammatory response. Leucocytes (mainly neutrophils) migrate from local vessels through the sulcular epithelium into the gingival sulcus. The gingival crevicular fluid (GCF) also contains complement, antibodies and other defence mechanisms. This is all part of the normal defence mechanism of healthy gingiva. Early gingivitis appears clinically as marginal inflammation: red colour and enlarged blood vessels. Moderate gingivitis is identified as marginal oedema ('rolled margins'). Severe gingivitis is less common and moves beyond a normal response. It is characterised by epithelial ulceration and indicates there is a more serious problem than plaque-induced gingivitis.

Periodontitis, or inflammation of the periodontal ligament, occurs when the protective gingiva has failed. This is overt disease. When the gingival epithelial attachment is destroyed, PDL and bone are damaged as the physiological sulcus deepens and converts to a pathological periodontal pocket. The lining sulcular epithelium changes into a very different pocket epithelium. Bacteria and bacterial by-products such as lipopolysaccharide stimulate local production and release of pro-inflammatory cytokines. Production of matrix metalloproteinases and PGE-2 is increased. The pro-inflammatory cytokines stimulate and attract neutrophils to migrate into the GCF, GCF quantity increases, the gingiva bleeds more easily and bone and supportive tissues are destroyed.

Treatment

Plaque consists of bacteria and bacterial by-products. Where supragingival plaque contacts the marginal gingiva, gingivitis is elicited as a normal response to antigenic stimulation. Both gingivitis and normal plaque may even be protective, helping to control proliferation of periodontopathogens. However, accumulated plaque quickly mineralises to form calculus ('tartar'), which when extensive, contributes to an environment that encourages the growth of subgingival plaque. In susceptible individuals, pathogenic subgingival plaque bacteria can overwhelm the local defenses resulting in periodontitis. Tissue damage results from the host response to the bacteria. This has been likened to 'a battleground destroyed in the battle'. A more accurate analogy may be that it is like the patient attempting to win the battle by eliminating the prize sought by the invaders (tooth exfoliation).

Since plaque directly causes gingivitis, plaque removal alone treats and prevents gingivitis. A clean tooth surface develops pellicle, a thin film of salivary glycoproteins, within minutes. Pioneering species of bacteria, typically gram-positive organisms (often Actinomyces and streptococci in dogs and cats) express adhesins that bind to the salivary glycoproteins. As the plaque biofilm thickens and matures, the community actively attracts new residents and provides an environment that is conducive to the growth of anaerobes and gram-negative organisms. Within days mature plaque is visible. When calculus is present, a professional dental scaling and polishing (PDSP) is indicated. Although calculus is not an active gingival irritant like plaque, it may act as a local passive gingival irritant and it provides a plaque-retentive surface.

Without treatment, periodontitis is irreversible; regrowth of normal cementum, PDL and alveolar bone cannot occur without intervention. Early periodontitis can be effectively treated with PDSP, returning the site to a non-active status. Although the attachment loss may not repair, the disease is held in remission. PDSP requires general anaesthesia and tracheal intubation with an inflated cuff to protect the patient from inhaling or aspirating aerosolised or dislodged debris. First plaque is removed by brushing and flushing with 0.12% chlorhexidine to decrease the amount of bacteria that are aerosolised during ultrasonic scaling. Then the teeth are scaled using a sonic or ultrasonic scaler. A curette is used to scale and plane the roots subgingivally and to debride any pocket epithelium. Finally the teeth are polished and flushed. A plaque attachment inhibitor can be applied to delay plaque reaccumulation.

Mild periodontitis (pocket depth up to one-third the length of the root) requires closed root planing and flushing. Placement of a locally active antibiotic implant (doxycycline, chlorhexidine, minocycline etc.) material may be helpful. Moderate periodontitis (periodontal pocket depth of up to two-thirds the length of the root) or pockets 5 mm or greater generally need open periodontal surgery to adequately clean the root surface under direct visualisation. In these cases, placement of a space-maintaining osseoconductive or osseoinductive material covered by an epithelial downgrowth inhibitor (guided bone regeneration/guided tissue regeneration (GBR/ GTR)) is the treatment of choice. Teeth with severe periodontitis (pocket depth of greater than two-thirds the length of the root) can also be treated with GBR/GTR. However, if the tooth is mobile the best treatment is extraction. Endodontic health must also be considered since periodontal infection can infect the pulp through lateral canals or apical foramina or canaliculi.

Systemic Antibiotics

Although systemic antibiotics can decrease the numbers of bacteria in the oral cavity due to their effect on the gingiva and in the saliva, this is an indirect route to the bacteria and decreases beneficial as well as pathogenic organisms. Brushing with a toothbrush more effectively and more directly removes the bacteria in plaque. Systemic antibiotics are recommended for treating deep periodontal or oral infections after mechanical and surgical treatment, and in very specific circumstances they are used prophylactically in anticipation of bacteraemia induced by oral manipulations. Indiscriminate use of antibiotics can encourage populations of resistant pathogenic bacteria and eliminate beneficial bacteria.

The bacteraemia that occurs during routine dental cleaning is not severe (on the order of 1-10 colony forming units or CFUs per ml of blood), lasts less than 1 hour and should be easily handled by an immunocompetent animal with no other predisposing factors. This level of bacteraemia is similar to that which occurs during normal mastication in which bacteria enter the bloodstream at a predicted cumulative rate of about 1000 times greater than that which occurs during a tooth extraction. Therefore most routine dental cleaning procedures do not require antibiotic administration. The American Dental Association, the American Academy of Oral Medicine and the Council on Scientific Affairs advise against the routine use of antibiotics for dental cleaning procedures.

Indications for perioperative antibiotics include painful oral ulcerations, moderate-to-severe periodontitis, systemic disease which may be worsened by bacteraemia (turbulent blood flow due to heart valve lesions, chronic renal failure) and concurrent clean or clean-contaminated surgical procedures. In these cases antibiotics should be timed to allow a therapeutic blood level prior to inducing the bacteraemia and to last for 1 hour postoperatively. The best antibiotics for oral infections include amoxicillin-clavulanate, clindamycin, metronidazole and tetracycline/doxycycline.

Prevention

Gingivitis is prevented by plaque control. In most individuals, chronic untreated plaque and gingivitis have not been shown to cause or lead to periodontitis. Only susceptible dogs and cats will develop periodontitis. While it is impossible to determine which pets will have progressive disease and which will not, it is possible to identify predisposing factors and eliminate some of them.

Intrinsic factors that predispose an individual to periodontitis include crowding, malocclusion, age, head size and other breed-related factors, presence of specific plaque bacteria, anatomical developmental aberrations such as enamel pearls, enamel dysplasia or palatogingival grooves, host immunity, hormone imbalance and systemic diseases such as diabetes mellitus, nephritis, hepatitis and retroviral infection. While some of these are genetically or developmentally determined, others can be eliminated. Presence of factors that can not be eliminated would require the patient to receive a higher level of regular oral hygiene.

Extrinsic predisposing factors include periodontal foreign material (interproximal or sulcular hair, grass, wood etc.), poor home oral hygiene, eating a non-abrasive diet (foods with no dental benefits), parafunctional habits (fanatically chewing abrasive toys, dirt, or other objects that cause gingival recession), subgingival restoration margins, poor polishing of teeth or restorations, use of systemic medications and radiation therapy. All of these extrinsic factors are iatrogenic or behavioural and can be eliminated to prevent the development of periodontitis. Home oral hygiene to remove plaque and identify problems early is the most important part of any preventive programme. Client education about the importance and the techniques for providing home care must be considered as part of our professional patient care. Tooth brushing remains the proven most effective means of removing plaque and preventing gingivitis. Other products help to control plaque through abrasional chewing, antimicrobial activity, or both.

Summary

The time to treat gingivitis is immediately when diagnosed. Simple daily plaque removal with a toothbrush will resolve it. The time to treat periodontitis is... immediately when it is diagnosed. Early disease is treated by a professional dental scaling and polish, and more advanced disease requires more aggressive intervention. As with any disease, the longer treatment is delayed, the more aggressive will be the required treatment and the less successful it will be.