Page 189 - ONLINE PROCEEDING BOOK WSAVA 2017
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edema, spontaneous bleeding, 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 in ammation should be used to judge the need for professional therapy.
As gingivitis progresses to periodontitis, the oral in ammatory 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 may be identi ed 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:
There are numerous recognized potential local effects of periodontal disease including:
• Oral-nasal  stulas (ONFs)
• Class II perio-endo abscesses.
• Pathologic fractures
• Ocular disease and blindness
• Oral cancer.
• Osteomyelitis,
Severe systemic manifestations:
Systemic rami cations of periodontal disease are also well documented. The in ammation of the gingiva and periodontal tissues that allows the body’s defenses
to attack the invaders also allows these bacteria to
gain access to the body. It is important to note that
just established gingivitis (i.e. no attachment loss) is enough to create these systemic effects. In humans,
the periodontal surface area comprises a surface area the size of the palm of your hand. This is a large area
of infection for the body to deal with. However, if you consider the size of the mouth and teeth of a small breed dog in relation to their body, there is actually a far greater level of infection affecting these patients.
There are a plethora of studies both in the human and
An Urban Experience
veterinary literature which document a link between periodontal in ammation and organ dysfunction. Affected organs include the kidneys and liver, leading to decrease in function of these vital organs over time. Furthermore,
it has also been suggested that these bacteria can become attached to previously damaged heart valves (i.e. valvular dysplasia) and cause endocarditis, which in turn can result in intermittent infections, and potentially thromboembolic disease. Other studies have linked
oral bacteremias to cerebral and myocardial infarctions and other histological changes. Additional human
studies have linked periodontal disease to an increased incidence of chronic respiratory disease (COPD) as well as pneumonia. Oral bacteremias have also been linked to arthritis and adverse pregnancy affects.
There are many studies that strongly link periodontal disease to an increase in insulin resistance, resulting in poor control of diabetes mellitus as well as increased severity
of diabetic complications (wound healing, microvascular disease). Additionally, it has been shown that diabetes
is also a risk factor for periodontal disease. Periodontal disease and diabetes are currently viewed as having a bidirectional interrelationship where one worsens the other.
Most critically, periodontal disease is now associated with early mortality. In other words, humans with bad periodontal disease die earlier than those in good periodontal health. In fact, periodontal disease is now viewed as a higher risk factor for early death than smoking!
Conversely, proper therapy of periodontal disease has been shown to have bene cial effects on systemic maladies. The kidney, liver, and heart function have all been shown to improve when periodontal disease is properly treated. Further, glycemic control is increased in patients with good periodontal health.
PERIODONTAL THERAPY
Methods and products for periodontal disease treatment and prevention can be grouped into three distinct treatment areas: control infection (pathogen control), decrease the amount of in ammation and/or bone destruction by the host (host modulation), and re-grow lost bone (guided tissue regeneration).
PATHOGEN CONTROL
It is well known that periodontal disease is initiated by plaque bacteria. Therefore, the basis for periodontal therapy is, and likely always will, be plaque control. Proper plaque control is a four pronged attack based on the level of disease:
1. Dental prophylaxis
2. Home care
3. Periodontal surgery
4. Extraction
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