Periodontal disease is the result of the inflammatory processes that occur in the tissues supporting teeth, in response to bacterial accumulation (dental plaque) on teeth, which is ultimately responsible for a progressive loss of collagen attachment of the teeth to the underlying bone (Ximenez et al ., 2000). Dental biofilm is the villain in the pathogenesis of periodontal diseases. However genetic background, host and environmental factors are considered modulators of the severity and progress of periodontal infections (Ishikawa et al., 2004). Periodontal diseases initiation is triggered by bacterial colonization on the surfaces of teeth while the clinical manifestations of these infections are affected by the host factors. Bacterial specificity and pathogenicity as well as the ability of the host defense to cope with the developing infection may influence the distribution pattern and rate of disease progression (Loesche et al., 2001). Non surgical periodontal therapy consists of the mechanical periodontal debridement and oral health care instructions. These measures are directed to the reduction of the bacterial load and altering the microbial flora to create more healthy ecology (Okada and Murakami, 1998; Gemmell et al., 2004). Periodontal pathogens elicit signals in resident gingival cells or in immune cells infiltrating the gingival tissues that result in immune responses. These responses lead to either the successful removal of the pathogens or to hostmediated destruction of the periodontal tissues. In this respect, cytokines in inflamed periodontal tissues, which have been the focus of numerous studies, have been cited as being of major importance in periodontal disease progression (Okada and Murakami, 1998).