Introduction
Periodontal disease is the number one health problem in small animal patients. Recent studies report that 90% of dogs at just 1 year of age have some form of periodontal disease. However, there are generally little to no outward clinical signs of the disease process, and therefore, therapy typically comes very late in the disease. Consequently, periodontal disease may also the most undertreated disease in our patients. Additionally, unchecked periodontal disease has numerous local as well as systemic consequences.

Pathogenesis
Periodontal disease is generally described in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which the inflammation is confined to the gingiva. The gingival inflammation is created by plaque bacteria and may be reversed with a thorough dental prophylaxis and consistent homecare. Periodontitis is the later stage of the disease process and is defined as an inflammatory disease of the deeper supporting structures of the tooth (periodontal ligament and alveolar bone) caused by microorganisms. The inflammation results in the progressive destruction of the periodontal tissues, leading to attachment loss. This can be seen as gingival recession, periodontal pocket formation, or both. Mild to moderate periodontal pockets may be reduced or eliminated by proper plaque and calculus removal. However, periodontal bone loss is irreversible (without regenerative surgery). Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, which is made up almost entirely of oral bacteria, contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is basically plaque which has secondarily become calcified by the minerals in saliva. Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into the area known as the gingival sulcus (between the gingiva and the teeth or alveolar bone), it is called subgingival plaque. Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease. However, once the periodontal pocket forms, the effect of the supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease. The bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade tissues on their own, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation causes damage to the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis, i.e. the destruction of the attachment between the periodontal tissues and the teeth. In addition to directly stimulating inflammation, the bacterial metabolic byproducts also elicit an inflammatory response from the animal. The inflammation produced by the combination of the subgingival bacteria and the host response damages the soft tissue attachment of the tooth and decreases the bony support.

Clinical Features
Normal gingival tissues are coral pink in color (allowing for normal pigmentation), and have a thin, knife-like edge, with a smooth and regular texture. In addition, there should be no demonstrable plaque or calculus on the dentition. Normal sulcal depth in a dog is 0 to 3mm and in a cat is 0 to 0.5mm. The first clinical sign of gingivitis is erythema of the gingiva. This is followed by edema, gingival bleeding during brushing or after chewing hard/rough toys, and halitosis. Gingivitis is typically associated with calculus on the involved dentition but is primarily elicited by PLAQUE and thus can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. It is critical to remember that calculus itself is essentially non-pathogenic. Therefore, the degree of gingival inflammation (not the amount of calculus) should be used to judge the need for professional therapy. As gingivitis progresses to periodontitis, the oral inflammatory changes intensify. The hallmark clinical feature of established periodontitis is attachment loss. In other words, the periodontal attachment to the tooth migrates apically. As periodontitis progresses, alveolar bone is also lost. On oral exam, there are two different presentations of attachment loss. In some cases, the apical migration results in gingival recession while the sulcal depth remains the same. Consequently, tooth roots become exposed and the disease process is easily identified on conscious exam. In other cases, the gingiva remains at the same height while the area of attachment moves apically, thus creating a periodontal pocket. This form is typically diagnosed only under general anesthesia with a periodontal probe. It is important to note that both presentations of attachment loss can occur in the same patient, as well as the same tooth. As attachment loss progresses, alveolar bone loss continues, until tooth exfoliation in most cases. After tooth exfoliation occurs, the area generally returns to an uninfected state, but the bone loss is permanent. 

Severe local consequences
In addition to tooth loss, there are six proven local severe sequelae of severe periodontal disease. The most common of these local consequences is an oral-nasal fistula (ONF). ONFs are typically seen in older, small breed dogs (especially chondrodystrophic breeds); however, they can occur in any breed as well as felines. ONFs are created by the progression of periodontal disease up the palatal surface of the maxillary canines however; any maxillary tooth is a candidate. This results in a communication between the oral and nasal cavities, creating an infection (sinusitis). Clinical signs include chronic nasal discharge, sneezing, and occasionally anorexia and halitosis. Definitive diagnosis of an oronasal fistula often requires general anesthesia. development of a fistula, periodontal surgery with guided tissue regeneration can be performed to save the tooth. Another potential severe consequence of periodontal disease can be seen in multi-rooted teeth and is called a class II perio-endo abscess. This occurs when the periodontal loss progresses apically and gains access to the endodontic system, thereby causing endodontic disease via bacterial contamination. The endodontic infection subsequently spreads though the tooth via the common pulp chamber and causes periapical ramifications on the other roots. The third potential local consequence of severe periodontal disease is a pathologic fracture. These fractures typically occur in the mandible (especially the area of the canines and first molars), due to chronic periodontal loss, which weakens the bone in affected areas. This condition is again, most commonly seen in small breed dogs, mostly because their teeth (especially the mandibular first molar) are larger in proportion to their jaws as in comparison to large breed dogs. Pathologic fractures occur most commonly as a result of mild trauma, or during dental extraction procedures. However, some dogs have suffered from fractures while simply eating. Although this is typically considered a disease of older patients, this author has personally treated three cases in dogs less than three years of age. The fourth local consequence of severe periodontal disease results from inflammation close to the orbit which could potentially lead to blindness. The fifth local consequence is described in recent studies which have linked chronic periodontal disease to oral cancer.  

Severe systemic manifestations
Systemic ramifications of periodontal disease are also well documented, while there s no true cause and effect, and many are human studies, the affected organs/systems include:
• Animals and humans
- Cardiovascular
- Renal
- Liver
- Cognitive disfunction
- Increased inflammatory markers
• Humans
- Diabetes
- Adverse pregnancy effects
- COPD
- Neoplasia
- Early mortality

The cornerstone of periodontal therapy is a thorough dental prophylaxis. This MUST be performed under general anaesthesia including a properly inflated endotracheal tube. The prophylaxis should include the following steps.
Step 1: Pre surgical exam and consultation
Step 2: Supragingival cleaning
 Step 3: Subgingival plaque and calculus scaling
Step 4: Polishing
Step 5: Periodontal probing, oral evaluation, and dental charting
Step 6: Dental radiographs:
 Step 7: Treatment planning 

Home care
This is a very important part of periodontal therapy. A recent study has shown that periodontal pockets are re-infected within 2 weeks of a prophylaxis if homecare is not performed. Therefore, homecare must be discussed with each client following a prophylaxis. There are two divisions of homecare active and passive. They both can be effective if performed correctly, however active homecare is still the gold standard in homecare.

Periodontal Surgery
Any pockets greater than normal for the species are pathologic and in need of therapy. In the canine patient, pockets between 3 and 5 mm which do not have mobility or other issues are best treated with closed root planing and subgingival curettage. Pockets greater than 5-mm require direct visualization of the root surface for effective cleaning. Visualization is best accomplished via periodontal flap procedures. The final modality for the therapy of periodontal disease is extraction. While extreme, it is the only true cure. Without a commitment to homecare or routine professional cleanings, advanced periodontal surgery should likely not be attempted. Depending on the stage of periodontal disease, the involved teeth should be extracted.