INTRUDUCTION
Periodontitis is a chronic inflammatory disease that affects the tooth supporting tissue the periodontium. It
is the most frequent cause of tooth loss in the adult population (Batrovaet al., 2014). The etiology of the disease
is multifactorial and bacterial deposits play an essential role in the pathogenesis. The bacteria that are involved
in periodontitis accumulate in the subgingival plaque that comprises predominantly of G
has been implicated in chronic periodontitis (Mysaket al.,
emiological studies have established that periodontitis is a risk factor for cardiovascular disease (Beck
and Offenbacher, 2001). It may be assumed that dental plaque bacteria not only influence the oral cavity locally,
but may also contribute to the development of some serious systemic diseases (Batrova
prevalence of CVD in patients with periodontitis is 25- 50% higher than in healthy individuals. Sever tooth loss
likely to be due to periodontal disease may be predictor of CVD- silent cerebral infarct (Minn, 2013). Links
between periodontitis and atherosclerosis would be predicted based upon inflammatory mechanisms initiated by
bacteria associated with periodontal lesions, locally or systemically, that then influence the initiation or
agation of the atherosclerosis (Schenkein and Loos, 2015).
Immune response has been shown to play a crucial role in the initiation and progression of periodontal
disease. It is well known that cellular immunity is reported to play a protective or aggressiv
- Ghurabi, 2015). Since both periodontitis and CVD are known to be
inflammatory conditions, it has been proposed that inflammation due to the periodontal microorganisms, the
known etiological agents of periodontitis, accounts for the contribution of periodontitis to increased CVD risk
and severity (Schenkein and Loos, 2015).The systemic dissemination of periodontal pathogens from periodontal